Cardiovascular System

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Ejection of blood from the right ventricle will continue until ________.

Select one:

a. pressure in the pulmonary artery is greater than pressure in the right ventricle

b. pressure in the pulmonary artery is less than pressure in the right ventricle

c. pressure in the aorta is greater than pressure in the right ventricle

d. pressure in the aorta is less than pressure in the right ventricle

e. the pulmonary semilunar valve contracts, inducing closure


The ________ carries oxygenated blood to the left side of the heart.

Select one:

a. pulmonary artery

b. superior vena cava

c. pulmonary vein

d. inferior vena cava

e. aorta


Which of the following chambers has the thickest musculature?

Select one:

a. right ventricle

b. right atrium

c. both ventricles have equal thickness and are thicker than the atria

d. left atrium

e. left ventricle


What region of the cardiovascular system contains valves?

Select one:

a. both the heart and veins Correct

b. veins only

c. metarterioles only

d. the heart, metarterioles, and veins

e. heart only


The contractile activity of smooth muscle cells within ________ is primarily involved in the control of the organ blood flow and mean arterial pressure.

Select one:

a. veins

b. arteries

c. venules

d. capillaries

e. arterioles Correct


An increase in the volume of blood ejected from the heart, with no change in total peripheral resistance, would ________.

Select one:

a. elevate mean arterial pressure Correct

b. elevate central venous pressure

c. reduce the stretch on the aorta

d. reduce mean arterial pressure

e. elevate pulmonary venous pressure


In the circulatory system, the largest pressure drop occurs across ________.

Select one:

a. capillaries

b. arteries

c. veins

d. venules

e. arterioles


Net capillary fluid filtration is enhanced by:

Select one:

a. Increased precapillary resistance

b. Increased tissue hydrostatic pressure

c. Decreased capillary plasma oncotic pressure

d. Decreased venous pressure

e. a and b


Baroreceptors respond to ________, which is/are altered by mean arterial pressure.

Select one:

a. the partial pressure of oxygen within the blood

b. the changes in stretch of the blood vessel wall Correct

c. the rate that blood is flowing past the nerves

d. the metabolic byproducts formed within blood vessel walls

e. the compressive forces of pressure against the nerve endings


Which of the following is NOT altered within seconds to minutes of the baroreceptor reflex being activated?

Select one:

a. blood volume Correct

b. stroke volume

c. heart rate

d. total peripheral resistance

e. activity of the sympathetic nervous system


Q3. You see a patient in the emergency department who has been diagnosed previously with left sided heart failure. On this visit, she is having trouble breathing and her chest sounds like there is fluid in her lungs. What are the physiological mechanisms that might explain this observation

Q2. A patient has inflammation of the pericardium, which has led to the production of excess fluid in the pericardial sac (pericardial effusion). The pressure in the pericardial sac is now higher than normal (this is called cardiac tamponade). What do you predict will happen to the person’s blood pressure? Explain

Q1. A man with liver disease loses the ability to synthesize plasma proteins. What happens to the osmotic pressure of his blood? What happens to the balance between filtration and absorption in his capillaries

Location of the Heart

between the diaphram left and right lung

Covering of the Heart Wall

heart is covered by fibrous pericardium

Layers of Heart Wall

innermost layer is endocardioum middle layer is mycardium outer most layer is epicardium

Right chambers of the heart

Right atrium Right ventricle

Left chambers of the heart

Left atrium Left ventricle


the Receiving Chambers

Vessels entering right atrium

– Superior vena cava – Inferior vena cava – Coronary sinus

Vessels entering left atrium

– Right and left pulmonary veins

• Papillary muscles

project into the ventricular cavities

• Vessel leaving the right ventricle

– Pulmonary trunk

• Vessel leaving the left ventricle

– Aorta

Purpose of Heart Valves

Ensure unidirectional blood flow through the heart

Atrioventricular (AV) valves

Prevent backflow into the atria when ventricles contract When atrial pressure is higher than ventricular pressure, the AV valve opens Tricuspid (right) Mitral valve (left)

Chordae tendineae

anchor Atrioventricular valve cusps to papillary muscles

Semilunar valves

revent backflow into the ventricles when ventricles relax Aortic semilunar valve (right) Pulmonary semilunar valve (left) When ventricular pressure exceeds the blood pressure in the aorta and pulmonary trunk, the semilunar valves open

Right side

pump for the pulmonary circuit Vessels carry blood to and from the lungs

Left side

pump for the systemic circuit Vessels carry blood to and from all body tissues

Right Pathway of Blood Through the Heart

Right atrium –>tricuspid valve –>right ventricle Right ventricle –>pulmonary semilunar valve –>pulmonary trunk –>pulmonary arteries–> lungs

Left Pathway of Blood Through the Heart

Lungs –>pulmonary veins –>left atrium Left atrium–>bicuspid valve –>left ventricle Left ventricle –>aortic semilunar valve –>aorta Aorta –>systemic circulation

Pulmonary circuit

is a short, low-pressure circulation

Systemic circuit

blood encounters much resistance in the long pathways thick myocardiant to create a greater fource of contraction to pump the blood to the systemic circulation against that higher resistance

Cardiac muscle cells

striated, short, fat, branched, and interconnected held together by connective tissue (collagen and elastin fibers) T-tubules wide but less numerous; SR is simpler Numerous large mitochondria Microscopic Anatomy of Cardiac Muscle junctions between cells anchor cardiac cells Desmosomes prevent cells from separating during contraction Gap junctions allow ions to pass ensure the heart contracts as a unit

Contraction of the heart

Depolarization is rhythmic and spontaneous AP–> Voltage gates Ca channels open for Ca to enter–> summation of Ca sparks create Ca signal–> Ca ions bind to triponin—> contraction

Relaxtion of the heart

Ca unbinds with troponin–> pumped back to SR to be stored–> Ca exchanges with Na with antiporter

• Intrinsic cardiac conduction system

A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart

Sequence of Excitation 1

The sinoatrial (SA) node (pacemaker) generates impulses about 75 times/minute (sinus rhythm) – Depolarizes faster than any other part of the myocardium

Sequence of Excitation 2

Atrioventricular (AV) node – Smaller diameter fibers; fewer gap junctions – Delays impulses approximately 0.1 second – Depolarizes 50 times per minute in absence of SA node input

Sequence of Excitation 3

Atrioventricular (AV) bundle (bundle of His) – Only electrical connection between the atria and ventricles

Sequence of Excitation 4

Right and left bundle branches – Two pathways in the interventricular septum that carry the impulses toward the apex of the heart

Sequence of Excitation 5

– Complete the pathway into the apex and ventricular walls – AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

Extrinsic Innervation of the Heart

• Heartbeat is modified by the ANS • Cardiac centers are located in the medulla oblongata – Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons – Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves

Cardiac cycle

all events associated with blood flow through the heart during one complete heartbeat Flow of blood through the heart is controlled by pressure changes Blood flows from higher to lower pressure through an opening


contraction pressure inside chamber increases and there is emptying of blood


relaxation pressure inside chamber decreases and there is filling of blood

The duration of a cardiac cycle depends

heart rate. During a cardiac cycle of 0.8sec, the ventricles are in systole for 0.3sec and in diastole for 0.5sec.

Four phases of the cardiac cycle

1. Inflow Phase 2. Isovolumetric Contraction 3. Outflow Phase 4. Isovolumetric Relaxation

Inflow Phase

inlet valve open, outlet valve closed

Isovolumetric Contraction

both valves closed, no blood flow

both valves closed, no blood flow

Outflow Phase

outlet valve open, inlet valve closed

The Cardiac Cycle Step 1 –

all chambers relaxed. atria fill with blood from the veins. AV valves open between atria and ventricles. blood passively flows from atria to ventricles. ventricles expand to accommodate the blood. Semilunar valves are closed

The Cardiac Cycle Step 2

AP fires in the SA node atrial cells depolarize. atria contract (systole) Atrial pressure increases . blood from the atria move into ventricles, remaining blood.

The Cardiac Cycle Step 3

depolarization wave reaches ventricles, contract and pressure in ventricle rises.Ventricular pressure exceeds atrial pressure, AV valves shut- first heart sound ("lub"). ventricles contract, volume of blood in them remains the same (isovolumetric contraction), the atria are repolarizing and relaxing. When atrial pressure falls below the pressure in the veins, the atria fill with blood.

Isovolumetric Relaxation

both valves closed, no blood flow

volume of blood in each ventricle
at the end of ventricular diastole

end diastolic volume (EDV).

The Cardiac Cycle Step 4

As ventricles contract, they eventually produce enough pressure to open the semilunar valves and push blood into the arteries. The pressure created by ventricular contraction becomes the driving force for blood flow. The AV valves remain closed and the atria continue to fill.

The volume of blood in each ventricle at the end of ventricular systole is called

end systolic volume (ESV).

The Cardiac Cycle Step 5

ventricles begin to repolarize and relax. Ventricular pressure decreases. When ventricular pressure falls below arterial pressure, blood starts to flow backwards in the aorta and pulmonary trunk. This closes the semilunar valves and causes the dicrotic notch (brief rise in aortic pressure). This creates the second heart sound, S2 ("dup"). The ventricles continue to relax, but the volume of blood is not changing (isovolumetric relaxation)

The Cardiac Cycle Step 6

When ventricular pressure falls below atrial pressure, the AV valves open. Blood moves into the ventricles and the cycle has started again.

Cardiac Output

amount of blood pumped by each ventricle in one minute. CO = heart rate (HR) X stroke volume (SV)


number of beats per minute


volume of blood pumped out of a ventricle with each beat

Cardiac output at rest

HR (75 beats/min) × SV (70 ml/beat) = 5.25 L/min

Maximal Cardiac Output

4-5 times resting CO in nonathletic people may reach 35 L/min in trained athletes

Cardiac reserve

difference between resting and maximal CO

Stroke Volume

-Blood volume before contraction (EDV) – Blood volume after contraction (ESV)

Stroke Volume At rest

= 135ml – 65ml = 70ml can increase to 100ml during exercise

Regulation of Stroke Volume

Venous Return–> Volume of Blood in Ventricle before Contraction (EDV)–> Length of muscle fibers–> Force of Ventricular Contraction–> SV Sympathetic/Parasympathetic Activity–> Contractility (changes in Ca2+ influx)—>Force of Ventricular Contraction–>SV

Frank-Starling Law

It states that the heart will pump out whatever volume is delivered to it. If the heart is filled with more blood, the heart is stretched more–> end of the sarcomere to move out–> increase the distant that it will have to travel–> increase contraction force–> more blood leave the heart (high SV) describes the relationship between EDV and SV. If the EDV doubles, then stroke volume will double.

Venous Return is affected by

Skeletal muscle pump Respiratory pump Body Position Sympathetic Activity

Skeletal muscle pump

The skeletal muscle surrounding the veins contracts and increases blood flow back to the heart (increases EDV).

Respiratory pump

During inhalation, the diaphragm descends and abdominal pressure increases. The increasing pressure squeezes veins and moves blood towards the heart (increases EDV).

Body Position

Gravity opposes the return of blood from the feet to the heart during sitting or standing. This effect is lost when we lie down.

Sympathetic Activity

The veins are innervated by sympathetic nerves. Activation of the SNS will constrict veins and push more blood towards the heart

Parasympathetic nerves

Parasympathetic nerves innervate the atrial muscle. Sparse innervation to ventricular muscle. They release acetylcholine (ACh) onto muscarinic receptors. This weakens atrial contraction and reduces stroke volume. Parasympathetic nerves innervate the SA and AV nodes.They release acetylcholine (ACh) onto muscarinic receptors. This reduces the frequency of spontaneous depolarization at the SA node and decreases excitability at the AV node. Together, this reduces heart rate.

Sympathetic nerves

Sympathetic nerves innervate the atrial and ventricular muscle. They release noradrenaline onto β receptors on cardiac myocytes. This increases the force of contraction of the atria and ventricles and increases stroke volume. Sympathetic nerves innervate the SA and AV nodes. They release noradrenaline onto β receptors. This increases the frequency of spontaneous depolarization at the SA node and increases excitability at the AV node. Together, this increases heart rate.


Sympathetic activation causes the release of adrenaline from the adrenal medulla. Adrenaline enters the blood stream and is delivered to the heart where it binds to β receptors at the SA node to increase heart rate. Thyroxine (thyroid gland hormone) increases heart rate and enhances the effects of noradrenaline and adrenaline

Blood Plasma

90% water Proteins mostly produced by the liver 60% albumin,36% globulins, 4% fibrinogen Nitrogenous by-products of metabolism Nutrients Electrolytes Respiratory gases Hormones

Blood Composition

Plasma Formed elements Erythrocytes (red blood cells, or RBCs), Leukocytes (white blood cells, or WBCs), Platelets

Formed elements

WBC, RBC, platletes (cell fragments)

Formed elements which are complete cells

white blood cells


ratio of red blood cells to plasma as a percentage of the total blood volume

Most blood cells originate

in bone marrow and do not divide

Survivial duration of formed elements

a few days


contact tissue cells and directly serve cellular needs Endothelium with sparse basal lamina


carry blood away from the heart; oxygenated except for pulmonary artery Structure includes Tunica intima, tunica media, and tunica externa


carry blood toward the heart; deoxygenated except for pulmonary vein Structure includes Tunica intima, tunica media, and tunica externa Formed when venules converge Have thinner walls, larger lumens compared with corresponding arteries. Blood pressure is lower than in arteries. Thin tunica media and a thick tunica externa consisting of collagen fibers and elastic networks Called capacitance vessels (blood reservoirs); contain up to 65% of the blood supply


Central blood-containing space

Tunica intima

Inner layer Endothelium lines the lumen of all vessels in all blood vessels, larger in vessels with subendothelial connective tissue basement membrane In arteries and arterioles, the outer margin of the tunica intima is delimited by an internal elastic membrane

Tunica media

– Middle layer – Smooth muscle and sheets of elastin – Sympathetic vasomotor nerve fibers control vasoconstriction and vasodilation of vessels

Tunica externa (tunica adventitia)

– Outermost layer – Collagen fibers protect and reinforce – In larger muscular arteries, there is frequently an external elastic membrane separating the tunica adventitia from the tunica media – Larger vessels contain vasa vasorum to nourish the external layer

Conducting Arteries

Large thick-walled arteries with elastin in all three tunics Aorta and major branches Conduct blood at high pressure to the medium-sized arteries Large lumen offers low resistance Act as pressure reservoirs—expand when the ventricle pumps blood into them and recoil when the ventricle relaxes Assist with propelling blood forward

Muscular (Distributing) Arteries and Arterioles

Distal to elastic arteries Deliver blood to body organs Have thick tunica media with more smooth muscle and fewer elastic fibers Active in vasoconstriction and vasodilation to adjust rate of blood flow


Smallest arteries Lead to capillary beds Control flow into capillary beds via vasodilation and vasoconstriction Regulate resistance to blood flow Regulate flow into capillaries (when tissue demand for O2 is high, the VSMCs relax and flow to the tissues increases.)


Microscopic exchange blood vessels Walls of thin tunica intima, one cell thick Pericytes within the basal lamina help stabilise their walls and control permeability Size allows only a single RBC to pass at a time In all tissues except for cartilage, epithelia, cornea and lens of eye Exchange gases, nutrients and waste products

Three structural types of Capillaries

1. Continuous capillaries 2. Fenestrated capillaries 3. Sinusoidal capillaries (sinusoids

Continuous capillaries

Abundant in the skin and muscles – Tight junctions connect endothelial cells – Intercellular clefts allow the passage of fluids and small solutes Continuous capillaries of the brain – Tight junctions are complete, forming the blood-brain barrier

Fenestrated capillaries

Some endothelial cells contain pores (fenestrations) More permeable than continuous capillaries Function in absorption or filtrate formation (small intestines, endocrine glands, and kidneys)

Sinusoidal Capillaries

Fewer tight junctions, larger intercellular clefts, large lumens Usually fenestrated Allow large molecules and blood cells to pass between the blood and surrounding tissues Found in the liver, bone marrow, spleen

Capillary Beds

Interwoven networks of capillaries form the microcirculation between arterioles and venules Consist of two types of vessels 1. Vascular shunt (metarteriole—thoroughfare channel): 2. True capillaries

Vascular shunt

• Directly connects the terminal arteriole and a postcapillary venule • Contains precapillary sphincters that open or close, thereby allowing different parts of the capillary bed to be perfused Usually only a small part of the capillary bed is perfused, except when a tissue becomes active

True capillaries

• 10 to 100 exchange vessels per capillary bed • Tissues with high metabolic activity have more capillaries • Branch off the metarteriole or terminal arteriole


Formed when capillary beds unite Very porous; allow fluids and WBCs into tissues Postcapillary venules consist of endothelium and a few pericytes Larger venules have one or two layers of smooth muscle cells

Capillary exchange

Capillaries allow for exchange of substances between the blood and interstitial fluid (extracellular fluid that surrounds the cells of the tissue).

Adaptations of capillaries that ensure return of blood to the heart

1. Large-diameter lumens offer little resistance 2. Valves prevent backflow of blood • Most abundant in veins of the limbs

Venous sinuses

flattened veins with extremely thin walls (e.g., coronary sinus of the heart and dural sinuses of the brain)

Pinocytosis in cappilaries

Plasma membrane invaginates and pinches off to capture large charged molecules (eg. proteins)

Diffusion via fenestration in cappilaries

Movement of water and solutes is driven by concentration gradient.

Diffusion across endothelial cell in cappilaries

Lipid soluble substances diffuse through the membrane (eg O2 and CO2)

Bulk flow (2 and 3) in cappilaries

Water and solutes can move from the blood in the capillary through fenestrations and clefts between cells. Plasma proteins normally cannot cross capillary walls (except in sinusoid capillaries). Bulk flow is driven by blood pressure and osmotic pressure.

Exchange can occur across the capillary in
four ways:

Pinocytosis Diffusion across endothelial cells or via fenestrations Bulk flow

Fluid Movement

The physical forces that govern the movement of fluid into and out of capillaries are called Starling Forces. These forces come from pressures. Capillary blood pressure drives fluid out of the capillaries. Blood also contains proteins (albumin and globulins) that create an osmotic pressure.

Hydrostatic pressur

mechanical pressure exerted on a membrane by a fluid. Here, the fluid is causing the pressure. Higher hydrostatic pressure leads to a higher pushing pressure of fluid.

Osmotic Pressure

the pulling pressure based on particles within a fluid. Here, the particles are causing the pressure. Higher osmotic pressure leads to a higher pulling pressure of fluid.

Filtration – Fluid is pushed out of the capillary by:

1. Hydrostatic pressure (blood pressure) in the capillary (HPc) 2. Osmotic Pressure in the interstitial fluid (OPif) Blood pressure in the capillary decreases along the length of the capillary because blood pressure drops. HPc at the arterial end of the capillary is ~35mmHg HPc at the venous end of the capillary is ~17mmHg Osmotic Pressure in the interstitial space is low due to low protein content (~1mmHg). It remains the same along the length of the capillary.

Reabsorption – Fluid is pulled into the capillary by:

1. Hydrostatic Pressure in the interstitial fluid (HPif) 2. Osmotic Pressure in the capillary (OPc~26) Hydrostatic pressure in the interstitial fluid is minimal, ranging from slightly negative to slightly positive because fluid is normally removed by the lymphatic system. Most textbooks use 0 mmHg. Osmotic pressure in the capillary is the pressure due to the presence of nondiffusible plasma proteins that draw fluid into the capillary from the interstitial space. The average value of OPc is 26mmHg. Little change occurs along the capillary from the arterial to the venous end.

Net Filtration Pressure

Comprises all the forces acting on a capillary bed At the arterial end of the capillary bed, hydrostatic forces dominate At the venous end of the capillary bed, osmotic forces dominate Excess fluid is returned to the blood via the lymphatic system results in a net LOSS of fluid from capillary to interstitial fluid: 10mmHg loss from capillary at the arterial end -8mmHg gain to capillary at the venous end 2mmHg net LOSS along the length of the capillary The excess fluid is returned to the blood stream via the lymphatic system.

Net Filtration Pressure At the arterial end:

Forces OUT = HPc + OPif = 35mmHg + 1 = 36mmHg Forces IN = HPif + OPc = 0 + 26mmHg = 26mmHg Net Filtration Pressure = [Forces OUT] – [Forces IN] Net Filtration Pressure = 36mmHg – 26mmHg = 10mmHg (flow OUT of capillary at arterial end)

Net Filtration Pressure At the venous end:

Forces OUT = HPc + OPif = 17mmHg + 1mmHg = 18mmHg Forces IN = HPif + OPc = 0mmHg + 26mmHg = 26mmHg Net Filtration Pressure = [Forces OUT] – [Forces IN] Net Filtration Pressure = 18mmHg – 26mmHg = -8mmHg (flow INTO capillary at venous end)

Lymphatic System

Returns interstitial fluid and leaked plasma proteins back to the blood Together with lymphoid organs and tissues, provide the structural basis of the immune system

Lymphatic vessels

start as blind-ended tubes and join together to form large lymphatic vessels. They join to the large veins andreturn the fluid to the circulation. This helps to maintain normal blood volume and pressure Lymphatic vessels are structurally similar to veins and capillaries. thin-walled contain one-way valves. holes between endothelial cells to allows movement of fluid and small proteins from interstitial space into the lymph vessels. Once interstitial fluid enters the lymphatic vessels, it is called lymph. only carry fluid away from the tissues no pump movement occurs through skeletal muscles, pressure changes in the thorax in breathing, contraction of smooth muscle in nearby arteries


At steady state, filtration equals reabsorption plus lymph flow. Under certain conditions, more fluid leaks out of capillaries than can be reabsorbed or collected by lymph vessels. The retention of fluid in the interstitial space is called edema. Edema occurs when the rate of filtration exceeds the sum of the rate of fluid reabsorption and lymphatic flow.

Special Circulations – Coronary Circulation

The coronary circulation supplies blood to the working heart muscle. The left main coronary artery arises from the aorta, travels behind the pulmonary artery and branches into the circumflex artery and left anterior descending artery (LAD). The circumflex and LAD artery supply blood to the left ventricle. The right main coronary artery arises from the aorta, travels behind the right atrium and ventricle toward the posterior regions of the heart to supply the right ventricle and atrium. These arteries are on the surface of the heart. They divide into smaller branches that dive into the myocardium. These resistance vessels regulate coronary blood flow. Coronary veins are adjacent to the coronary arteries. These veins drain into the coronary sinus which empties into the right atrium. During systole, the contraction of the myocardium compresses the small coronary vessels within the ventricular wall, thereby increasing resistance and decreasing flow. During diastole, the compressive forces are removed and blood flow increases. Coronary blood flow reaches a peak in early diastole and then falls passively as the aortic pressure falls toward its diastolic value. Thus, it is the aortic pressure during diastole that is crucial for perfusing the coronary arteries

Blood flow

Volume of blood flowing through a vessel, an organ or the entire circulation in a given period of time. In the entire circulation, blood flow is equal to the cardiac output (relatively constant at rest). Blood flow through individual organs can vary depending upon need. Blood flow (F) is directly proportional to the blood pressure gradient (P) – If P increases, blood flow speeds up Blood flow is inversely proportional to peripheral resistance (R) – If R increases, blood flow decreases: F = P/R

Blood Velocity

The distance per unit time with which blood flows through a given segment of the circulation. Varies throughout the vasculature and is inversely proportional to the total cross-sectional area. The velocity of flow is slowest in the capillaries which allows time for exchange of nutrients and wastes.

Blood pressure (BP)

Force per unit area exerted on the wall of a blood vessel by the blood • Expressed in mm Hg • Measured as systemic arterial BP in large arteries near the heart – The pressure gradient provides the driving force that keeps blood moving from higher to lower pressure areas


Resistance (peripheral resistance) – Opposition to flow – Measure of the amount of friction blood encounters – Generally encountered in the peripheral systemic circulation R is more important in influencing local blood flow because it is easily changed by altering blood vessel diameter If the expression for resistance is combined with the equation describing the relationship between flow, pressure and resistance (Flow = P/R), the following is obtained: Poiseuille’s Equation:

Three important sources of resistance

– Blood viscosity () – Total blood vessel length (L) – Blood vessel diameter (r)

– Blood viscosity (n)

• The "stickiness" of the blood due to formed elements and plasma proteins

– Total blood vessel length (L)

• The longer the vessel, the greater the resistance encountered

– Blood vessel diameter (r)

• the smaller the radius, the greater the resistance • resistance varies inversely with the fourth power of vessel radiu

Resistance equation

Resistance =(n*L)/ r^4

Systemic Blood Pressure

The pumping action of the heart generates blood flow Pressure results when flow is opposed by resistance Systemic pressure – Is highest in the aorta – Declines throughout the pathway – Is 0 mm Hg in the right atrium The steepest drop occurs in arterioles

Poiseuille’s Equation:

Flow =(delta GP r^4) / 8 n L

Arterial Blood Pressure

Reflects two factors of the arteries close to the heart – Elasticity (compliance or distensibility) – Volume of blood forced into them at any time Blood pressure near the heart is pulsatile Mean arterial pressure (MAP): pressure that propels the blood to the tissues MAP = diastolic pressure + 1/3 pulse pressure Pulse pressure and MAP both decline with increasing distance from the heart

Capillary Blood Pressure

Ranges from 15 to 35 mm Hg Low capillary pressure is desirable – High BP would rupture fragile, thin-walled capillaries – Most are very permeable, so low pressure forces filtrate into interstitial spaces

Venous Blood Pressure

Changes little during the cardiac cycle Small pressure gradient, about 15 mm Hg Low pressure due to cumulative effects of peripheral resistance

What is Flow in the Systemic Circulation?

Blood Flow = CO Cardiac Output (CO) is the amount of blood pumped by each ventricle in one minute.

What is Pressure Gradient in the Systemic Circulation?

P1 = Parterial P2 = Pvenous In practice, venous pressure is usually small enough to be neglected, therefore ΔP ~ Parterial PGradient = P1 – P2 = Parterial – Pvenous ~ MABP

What is Resistance in the Systemic Circulation?

The majority of the resistance in the systemic circulation comes from the resistance in the arterioles. This resistance is called systemic vascular resistance (SVR) or total peripheral resistance (TPR).

How Blood Volume Affects Blood Pressure

An increase in blood volume will increase CVP, EDV and stroke volume (Frank- Starling Law). An increase in stroke volume then increases cardiac output and arterial blood pressure. MABP = SV x HR x SVR MABP = CO x SVR

The main factors influencing blood pressure:

– Cardiac output (CO) – Total peripheral resistance (TPR) – Blood volume

Control of Blood Pressure

Short-term neural controls Long-term renal regulation

Short-term neural controls

– Counteract fluctuations in blood pressure by altering peripheral resistance Baroreceptor Chemoreceptors

Long-term renal regulation

– Counteracts fluctuations in blood pressure by altering blood volume


located in – Carotid sinuses – Aortic arch – Walls of large arteries of the neck and thorax They relay information back to the brain At rest, arterial baroreceptor activity tonically inhibits sympathetic outflow to the heart and blood vessels and it tonically stimulates vagal outflow to the heart.

Chemoreceptors Initiated

located in the – Carotid sinus – Aortic arch – Large arteries of the neck Chemoreceptors respond to rise in CO2, drop in pH or O2 – Increase blood pressure via the vasomotor center and the cardioacceleratory center Are more important in the regulation of respiratory rate

Short-term Regulation of Blood Pressure Sympathetic neurons

Sympathetic neurons innervate veins, arterioles and the heart (SA node and myocytes). Output from the SNS act on arterioles to change systemic vascular resistance (SVR). Peripheral blood vessels are in a state of partial (rather than full) constriction

Short-term Regulation of Blood PressureParasympathetic neurons

Parasympathetic neurons innervate the SA node.

Following an increase in BP:

– increased pressure stretches the baroreceptors – increased afferent nerve firing – more activation of PNS → ↓HR – more inhibition of SNS → ↓HR and ↓contractility → ↓SV – more inhibition of SNS → ↓constriction of arterioles → ↓SVR – ↓MABP since MABP = CO X SVR

Following a decrease in BP:

– decreased stretching of baroreceptors – decreased afferent nerve firing – less activation of PNS → ↑HR – less inhibition of SNS → ↑ HR and ↑ contractility → ↑ SV – less inhibition of SNS → ↑ vasoconstriction→ ↑ SVR – ↑ MABP since MABP = CO X SVR

Hormonal Controls

Adrenaline, released by the adrenal medulla, causes generalised vasoconstriction and increase cardiac output Angiotensin II, generated by kidney release of renin, causes vasoconstriction Antidiuretic hormone (ADH or vasopressin) causes intense vasoconstriction in cases of extremely low BP Atrial natriuretic peptide causes blood volume and blood pressure to decline, causes generalised vasodilation Antidiuretic hormone (ADH or vasopressin) causes intense vasoconstriction in cases of extremely low BP

Long Term Mechanisms Of Renal System

Baroreceptors quickly adapt to chronic high or low BP Long-term mechanisms step in to control BP by altering blood volume Kidneys act directly and indirectly to regulate arterial blood pressure 1. Direct renal mechanism 2. Indirect renal (renin-angiotensin) mechanism

1. Direct renal mechanism

Alters blood volume independently of hormones – Increased BP or blood volume causes the kidneys to eliminate more urine, thus reducing BP – Decreased BP or blood volume causes the kidneys to conserve water, and BP rises

Indirect Mechanism

The renin-angiotensin mechanism – Arterial blood pressure release of renin – Renin production of angiotensin II – Angiotensin II constricts arterioles (↑ SVR) The renin-angiotensin mechanism – Angiotensin II aldosterone secretion • Aldosterone renal reabsorption of Na+ and urine formation (↑ blood volume) – Angiotensin II stimulates ADH release leading to water reabsorption by kidneys (↑ blood volume) – ↑ MABP

Regulation of Vascular Resistance

Tissues attempt to adjust blood flow to their own needs by changing the diameter of their resistance vessels. Resistance vessels can be regulated by different mechanisms: Local control – metabolic – myogenic Central control – innervation of the sympathetic nervous system Hormonal control – the release of circulating hormones modulate resistance vessels

Regulation of Vascular Resistance: Metabolic Controls

Vasodilation of arterioles and relaxation of precapillary sphincters occur in response to – Declining tissue O2 – Substances from metabolically active tissues (H+, K+, adenosine, and prostaglandins) and inflammatory chemicals Effects – Relaxation of vascular smooth muscle – Release of NO from vascular endothelial cells Nitric oxide is the major factor causing vasodilation Vasoconstriction is due to sympathetic stimulation and endothelin

Regulation of Vascular Resistance: Metabolic Control Nitric oxide

– potent vasodilator – NO mediates the actions of ACh, Substance P, ATP, bradykinin and flow-induced shear stress.

Regulation of Vascular Resistance: Metabolic Control Prostaglandins

– are synthesized from arachidonic acid – PGE (PGE1, PGE2 and PGE3) and PGI2 (prostacyclin) relax VSMCs – PGF (PGF1, PGF2a, PGF3a) and thromboxane A2 are vasoconstrictors

Regulation of Vascular Resistance: Metabolic Control Endothelium-derived hyperpolarization (EDH)

opens K+ channels on VSMCs – causes hyperpolarization and vasodilation

Regulation of Vascular Resistance: Metabolic Control Endothelins

– are synthesized and released by endothelial cells in response to Ang-II and mechanical trauma – ET1 binds to ETA receptors on VSMCs and causes vasoconstriction

Regulation of Vascular Resistance: Myogenic Controls

Myogenic responses of vascular smooth muscle keep tissue perfusion constant despite most fluctuations in systemic pressure Passive stretch (increased intravascular pressure) promotes increased tone and vasoconstriction Reduced stretch promotes vasodilation and increases blood flow to the tissue

Regulation of Vascular Resistance: Central Control

All resistance vessels (arterioles) are innervated by the sympathetic nervous system. When arterial pressure falls, SNS nerve terminals release noradrenaline onto the VSMCs, causing them to contract. This causes vasoconstriction and a decrease in flow.

Regulation of Vascular Resistance Hormonal Control

Antidiuretic hormone (ADH) Angiotensin II (Ang-II) Adrenaline

Antidiuretic hormone (ADH)
ADH (aka arginine vasopressin, AVP) Regulation of Vascular Resistance Hormonal Control

released from the posterior pituitary when blood pressure decreases or tissue osmolarity rises. ADH binds to ADH V1 receptors leading to vasoconstriction.

Angiotensin II (Ang-II) Regulation of Vascular Resistance Hormonal Control

Ang-II appears in the bloodstream when renal artery pressure falls. SNS activity can also trigger Ang-II release. Ang-II is a potent vasoconstrictor

Adrenaline Regulation of Vascular Resistance Hormonal Control

Sympathetic stimulation secretes adrenaline from the adrenal medulla. Adrenaline enters the blood stream. The binding of adrenaline on receptors (on all arterioles) leads to vasoconstriction. The binding of adrenaline on 2 receptors (on arterioles of skeletal muscle and heart) leads to vasodilation.

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