Chapter 13&14 lecture-1

Chapters 13 & 14

Blood, Heart, and Circulation

Lecture PowerPoint

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Overview

13-3

Circulatory System Components

• Cardiovascular system– Heart: four-chambered pump– Blood vessels: arteries, arterioles, capillaries,

venules, and veins

• Lymphatic system– Lymphatic vessels, lymphoid tissues,

lymphatic organs (spleen, thymus, tonsils, lymph nodes)

Circulatory System Functions

• Transportation– Respiratory gases, nutrients, and wastes

• Regulation– Hormonal and temperature

• Protection– Clotting and immune

I. Composition of the Blood

Composition of the Blood

1. Plasma: fluid part of blood– Plasma proteins– Serum


1. Plasma: fluid part of blood •Nutrients and metabolites

– Glucose, amino acids, fatty acids etc

•Hormones– Insulin, glucagon, sex hormones etc.

•Ions– Na+ (major ion; maintains osmotic pressure)– K+, Ca++, Cl-, Mg++ etc

•Bicarbonate; important buffer

•Respiratory gasses– O2, CO2

•Waste products– Urea, food additives etc.


Plasma: fluid part of blood (Continued)• Proteins constitute 7-9% of plasma• Three types of plasma proteins: albumins, globulins, &

fibrinogen– Albumin accounts for 60-80% (Major protein)

• Creates colloid osmotic pressure that draws H20 from interstitial fluid into capillaries to maintain blood volume & pressure

– Globulins • Alpha and beta globulins transport lipid soluble molecules• Gamma globulins are antibodies (fight infection)

– Fibrinogen • a soluble protein that functions in clotting• Converted to fibrin; an insoluble protein polymer• Serum is fluid left when blood clots (plasma minus fibrinogen)


2. Formed Elements

GranulocytesNeutrophilsEosinophilsBasophils

AgranulocytesLymphocytesMonocytes


2. Erythrocytes

– Carry oxygen

– Lack nuclei and mitochondria

– Have a 120-day life span

– Contain hemoglobin and transferrin



• 3. Leukocytes• Have nucleus, mitochondria, & amoeboid ability • Can squeeze through capillary walls (diapedesis)

– Granular leukocytes help detoxify foreign substances & release heparin• Include eosinophils, basophils, & neutrophils

13-10


• 3. Leukocytes (Contd)

• Agranular leukocytes are phagocytic & produce antibodies

• Include lymphocytes & monocytes

13-11


4. Platelets (thrombocytes)

- Smallest formed element

– Lack nuclei

- Very short-lived (5−9 days)- Clot blood- Need fibrinogen

Formed Elements in the Blood

Hematopoiesis

• Is formation of blood cells from stem cells in bone marrow (myeloid tissue) & lymphoid tissue

• Erythropoiesis is formation of RBCs– Stimulated by erythropoietin (EPO) from kidney

• Leukopoiesis is formation of WBCs– Stimulated by variety of cytokines

• = autocrine regulators secreted by immune system13-13

Erythropoiesis

• 2.5 million RBCs are produced/sec

• Lifespan of 120 days

• Old RBCs removed from blood by phagocytic cells in liver, spleen, & bone marrow– Iron recycled

back into hemoglobin production

13-14

Blood Clotting

• Hemostasis: cessation of bleeding when a blood vessel is damaged

• Damage exposes collagen fibers to blood,

producing:

1. Vasoconstriction

2. Formation of platelet plug

3. Formation of fibrin protein web

Blood Clotting: Platelets

• Platelets don't stick to intact endothelium because of presence of prostacyclin (PGI2--a prostaglandin) & NO– Keep clots from

forming & are vasodilators

13-20

QuickTime™ and aTIFF (LZW) decompressor

are needed to see this picture.

Consequences of Blood Clotting in Normal Vessels


• Damage to endothelium allows platelets to bind to exposed collagen– von Willebrand factor

increases bond by binding to both collagen & platelets

– Platelets stick to collagen & release ADP, serotonin, & thromboxane A2

• = platelet release reaction

13-21

Damaged blood vessel wall


• Some chemicals (serotonin & thromboxane A2) stimulate vasoconstriction, reducing blood flow to wound

• Other chemicals (ADP & thromboxane A2) cause other platelets to become sticky & attach & undergo platelet release reaction– This aggregation

continues until platelet plug is formed

13-22

Platelet aggregation

Blood Clotting: Fibrin

• Next, calcium and phospholipids (from the platelets) convert prothrombin to the active enzyme thrombin, which converts fibrinogen to fibrin.


• Fibrinogen is converted to fibrin via one of two pathways:1. Intrinsic: Activated by exposure to collagen

or glass which activates a cascade of other blood factors.


2. Extrinsic: Initiated by tissue factor (factor III). This is a more direct pathway.

• Vitamin K is needed for both pathways.

13-25

Intrinsic: Activated by exposure to collagen

Extrinsic: Initiated by tissue factor (factor III).

• Platelet plug becomes infiltrated by meshwork of fibrin• Clot now contains platelets, fibrin & trapped RBCs

– Platelet plug undergoes plug contraction to form more compact plug

Role of Fibrin

13-23


Anticoagulants

• Clotting can be prevented with certain drugs:

– Calcium chelators (sodium citrate or EDTA)

– Heparin: blocks thrombin

– Coumarin: inhibits vitamin K

Blood Clotting

Dissolution of Clots

• When damage is repaired, activated factor XII causes activation of kallikrein – Kallikrein converts plasminogen to plasmin

• Plasmin digests fibrin, dissolving clot

13-26

II. Structure of the Heart

Structure of the Heart• Right atrium: receives

deoxygenated blood from the body

• Left atrium: receives oxygenated blood from the lungs

• Right ventricle: pumps deoxygenated blood to the lungs

• Left ventricle: pumps oxygenated blood to the body

• Chambers separated by fibrous skeleton

Pulmonary and Systemic Circulations

• Pulmonary: between heart and lungs– Blood pumps to lungs via

pulmonary arteries.– Blood returns to heart via

pulmonary veins.• Systemic: between heart

and body tissues– Blood pumps to body

tissues via aorta.– Blood returns to heart via

superior and inferior venae cavae.

• Resistance in systemic circuit > pulmonary– Amount of work done by left ventricle pumping to systemic is

5-7X greater• Causing left ventricle to be more muscular (3-4X thicker)

Pulmonary & Systemic Circulations continued

13-34

Valves of the Heart

• Atrioventricular valves: located between the atria and the ventricles– Tricuspid: between

right atrium and ventricle

– Bicuspid: between left atrium and ventricle

Valves of the Heart

• Semilunar valves: located between the ventricles and arteries leaving the heart– Pulmonary: between

right ventricle and pulmonary trunk

– Aortic: between left ventricle and aorta

Valves of the Heart

• Opening & closing of valves results from pressure differences– High pressure of

ventricular contraction is prevented from everting AV valves by contraction of papillary muscles which are connected to AVs by chorda tendinea

13-37

Three Types of Muscle• Skeletal Muscle

– Voluntary

– Striated

– Not interconnected

– Long and not branched

• Cardiac Muscle– Involuntary

– Striated

– Interconnected via intercalated discs (Gap junctions)

– Functional syncytium

• Smooth Muscle– Involuntary– Non-striated– Most have gap junctions

• Pericardial Sac:

• Anchors the heart

• Reduces friction against the rib cage

Structure of Heart Wall

III. Electrical Activity of the Heart and the Electrocardiogram

Electrical Activity of the Heart• Cardiac muscle cells are interconnected by gap junctions

called intercalated discs.– Once stimulation is applied, it flows from cell to cell.– The area of the heart that contracts from one

stimulation event is called a myocardium.– The atria and ventricles are separated electrically by

the fibrous skeleton.

Electrical Activity of the HeartAutorhythmicity: Rhythmic beat of heart

produced by producing its own action potentials

Authorhythmic cells: Special cardiomyocytes that initiate and conduct action potentials

At −40mV, voltage-gated Ca2+

channels open, triggering action potential and contraction.

Repolarization occurs with the opening of voltage-gated K+ channels

Electrical Activity of the Heart

• Sinoatrial node: “pacemaker”; located in right atrium– Pacemaker potential: slow, spontaneous

depolarization


• Pacemaker cells in the sinoatrial node depolarize spontaneously, but the rate at which they do so can be modulated:

– Epinephrine and norepinephrine increase the heart rate.

– Parasympathetic neuron slows heart rate.

Electrical Activity of the Heart• Myocardial action potentials

– Cardiac muscle cells have a resting potential of −90mV.

– They are depolarized to threshold by action potentials from the SA node.

Voltage-gated Na+ channels open, and membrane potential plateaus at 15mV for 200−300 msec.

Due to balance between slow influx of Ca2+ and efflux of K+

More K+ are opened, and repolarization occurs.


– Action potentials spread via intercalated discs (gap junctions).

– AV node at base of right atrium and bundle of His conduct stimulation to ventricles.


– In the interventricular septum, the bundle of His divides into bundle branches.

– Branch bundles become Purkinje fibers, which stimulate ventricular contraction.


– Action potentials from the SA node spread rapidly.

• 0.8–1.0 meters/second– At the AV node, APs slow

down.• 0.03−0.05 m/sec• This accounts for half of

the time delay between atrial and ventricular contraction.

– The speed picks up in the bundle of His, reaching 5 m/sec in the Purkinje fibers.

– Ventricles contract 0.1–0.2 seconds after atria.

Spread of Excitation

Refractory Periods

• Because the atria and ventricles contract as single units, they cannot sustain a contraction.

• Because the action potential of cardiac cells is long, they also have long refractory periods before they can contract again.

Electrocardiogram

• This instrument records the electrical activity of the heart by picking up the movement of ions in body tissues in response to this activity.

Electrocardiogram

• P wave: atrial depolarization

• QRS wave: ventricular depolarization

• S-T segment: plateau phase

• T wave: ventricular repolarization

Electrocardiogram

Heart Sounds

• Produced by closing valves

- “Lub” = closing of AV valves• Occurs at ventricular systole

- “Dub” = closing of semilunar valves• Occurs at ventricular diastole

ECG and Heart Sounds

• Lub occurs after the QRS wave.

• Dub occurs at the beginning of the

T wave.

Heart Murmur

• Abnormal heart sounds produced by abnormal blood flow through heart. – Many caused by defective heart valves.

• Mitral stenosis: Mitral valve calcifies and impairs flow between left atrium and ventricle. – May result in pulmonary hypertension.

Heart Murmur

• Incompetent valves: do not close properly– May be due to damaged

papillary muscles

• Septal defects: holes in interventricular or interatrial septum – Blood crosses sides.

IV. Cardiac Cycle

Cardiac Cycle

• Repeating pattern of contraction and relaxation of the heart.

– Systole: contraction of heart muscles

– Diastole: relaxation of heart muscles

Cardiac Cycle

1. Ventricles begin contraction, pressure rises, and AV valves close (lub).

2. Pressure builds, semilunar valves open, and blood is ejected into arteries.

1. Pressure in ventricles falls; semilunar valves close (dub).

Cardiac Cycle

4. Pressure in ventricles falls below that of atria, and AV valve opens. Ventricles fill.

5. Atria contract, sending last of blood to ventricles

Cardiac Cycle and Pressures

V. Blood Vessels

Blood Vessels

• Arteries

• Arterioles

• Capillaries

• Venules

• Veins

Parallel Arrangement of Blood Flow

Allows:All organs to receive blood of same compositionBlood flow through an organ system to be adjusted according to need

Blood constantly reconditionedReconditioning organs (digestive organs, Kidneys, Skin) receive more blood than their own need

Blood Vessels

73

Table 13.8

Blood Vessels• Innermost layer of all vessels is

the endothelium

• Capillaries are made of only endothelial cells

• Arteries & veins have 3 layers called tunica externa, media, & interna

– Externa is connective tissue

– Media is mostly smooth muscle

– Interna is made of endothelium, basement membrane, & elastin

• Although have same basic elements, arteries & veins are quite different

Arteries

• Large arteries are muscular & elastic– Contain lots of elastin so very elastic– Expand during systole & recoil during diastole

• Helps maintain smooth blood flow during diastole• Serve as rapid transit pathway to the tissues and pressure reservoir

during diastole

13-67

Arterioles• Small arteries & arterioles are muscular

– Provide most resistance in circulatory system– Arterioles cause greatest pressure drop– Mostly connect to capillary beds

• Some connect directly to veins to form arteriovenous anastomoses

13-68

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)

14-33

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 () and inversely proportional to 4th power of radius

So diameter of vessel is very important for resistance because viscosity and length of the vessel do not change

Mean Arterial Pressure: Diastolic Pressure (80) + 1/3rd Pulse Pressure (13.33) Pulse Pressure = Systolic Pressure (120) – Diastolic Pressure (80) So MAP for a normal BP is 80 + 13.33 = 93.33

14-34

Relationship between blood flow,

radius & resistance

14-35

Relationship between blood flow,

radius & resistance

Vasoconstriction and Vasodilation

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. Brain requires a constant supply of blood

14-39

• 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)

• Reactive hyperemia: a local vosodilation in response to stopping or constriction of blood flow to the area.

Intrinsic Regulation of Blood Flow (Autoregulation) continued

14-40

• Local Histamine Release: In injuries or allergies local histamine release causes vasodilation

• Local Heat or Cold: Used therapeutically to reduce vasodilation by applying cold packs to affected areas

Intrinsic Regulation of Blood Flow (Autoregulation) continued

14-40

• Sympathoadrenal activation (Neural Control) 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

Endocrine control: Many hormones affect the radii of arterioles; e.g., epinephine, angiotensin and vasopressin cause vasoconstriction

Extrinsic Regulation of Blood Flow

14-36

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

14-38

Aerobic Requirements of the Heart

• The coronary arteries supply blood to a massive number of capillaries (2,500–4,000 per cubic mm tissue). Heart is the most perfused tissue in human body

– Unlike most organs, blood flow is restricted during systole. Cardiac tissue therefore has myoglobin to store oxygen during diastole to be released in systole.

Circulatory Changes During Exercise

• Cardiac output can increase 5X due to increased cardiac rate.

• Stroke volume can increase some due to increased venous return.

Cerebral Circulation

• The brain cannot tolerate much variation in blood flow. – At high pressure, vasoconstriction occurs to

protect small vessels from damage and stroke.

– When blood pressure falls, cerebral vessels automatically dilate.

• Provide extensive surface area for exchange • Blood flow through a capillary bed is determined by state of

precapillary spincters of arteriole supplying it

Capillaries

13-69

• In continuous capillaries, endothelial cells are tightly joined together– Have narrow intercellular channels that permit exchange of

molecules smaller than proteins – Present in muscle, lungs, adipose tissue

• Fenestrated capillaries have wide intercellular pores– Very permeable– Present in kidneys, endocrine glands, intestines.

• Discontinuous capillaries have large gaps in endothelium• Are large & leaky• Present in liver, spleen, bone marrow.

Types of Capillaries

13-70

Exchange across capillary wall

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)

14-19

Fig 14.9

14-22

Cutaneous Blood Flow

• The skin can tolerate the greatest fluctuations in blood flow.

• The skin helps control body temperature in a changing environment by regulating blood flow = thermoregulation.– Increased blood flow to capillaries in the skin releases

heat when body temperature increases.– Sweat is also produced to aid in heat loss.– Vasoconstriction of arterioles keeps heat in the body

when ambient temperatures are low.

Cutaneous Blood Flow

• Thermoregulation is aided by arteriovenous anastomoses, which shunt blood from arterioles directly to venules.

• Contain majority of blood in circulatory system• Capicitance vessels• Very compliant (expand readily), but not elastic• Contain very low pressure (about 2mm Hg)

– Insufficient to return blood to heart– Have valves for one way flow

Veins

13-71

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

14-16

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

14-15

• Blood is moved toward heart by contraction of surrounding skeletal muscles (skeletal muscle pump) – & pressure drops

in chest during breathing

– 1-way venous valves ensure blood moves only toward heart

Venous Return

13-72

VI. Lymphatic System

Functions of the Lymphatic System

• Transports excess interstitial fluid (lymph) from tissues to the veins

• Produces and houses lymphocytes for the immune response

• Transports absorbed fats from intestines to blood

Lymphatic System continued

• Lymphatic capillaries are closed-end tubes that form vast networks in intercellular spaces– Very porous, absorb

proteins, microorganisms, fat

13-88

Vessels of the Lymphatic System

• Lymphatic capillaries: smallest; found within most organs– Interstitial fluids, proteins,

microorganisms, and fats can enter.

• Lymph ducts: formed from merging capillaries– Similar in structure to veins– Lymph is filtered through

lymph nodes

• Tonsils, thymus, spleen– Sites for lymphocyte

production

Organs of the Lymphatic System

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

14-23

107

108

Table 14.2

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

14-54

VII Cardiac Output

14-3

• Is volume of blood pumped/min by each ventricle

• Stroke volume (SV) = blood pumped/beat by each ventricle

• CO = SV (`70 ml/min) x HR (`70 beats/min) =4900ml/min

• Total blood volume is about 5.5L

Cardiac Output (CO)

14-4

Fig 14.5

14-14

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)

• Autonomic innervations of SA node is main controller of HR– Sympathetic NS increases heart rate by releasing

epinephrine and Nor-epinephrine– Parasympathetic NS innervates at the SA node

and releases Acetylcholine. The affect is to reduce the heart rate

14-5

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

14-9

• 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• Ejection fraction is SV/ EDV

– Normally is 60%; useful clinical diagnostic tool

Regulation of Stroke Volume

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 & SV

Fig 14.2

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 & contraction would be weak

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

14-12

Extrinsic Control of Contractility

• 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

14-13

14-14

VIII Blood Pressure

14-51

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

14-52

Blood Pressure (BP)

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

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

14-54

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

14-55

Fig 14.2614-56

14-57

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

14-58

Chapter 13&14 lecture-1

Documents

blood clotting hemostasis

formation of blood cells

blood clots plasma

days clot blood

blood continued proteins

blood flow towound

blood plasma proteins

chambered pump blood