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Bio241_chapter13_blood_lecture
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Bio241_chapter13_blood_lecture
Overview
Chapter focuses on
Blood, Heart, and Circulation
(BIOL 241 – Ch. 13)
Sub-topics: Blood • Pulmonary & Systemic Circulations • Heart Valves • Cardiac Cycle • Electrical Activity • Structure of Vessels
Functions of the Circulatory System
Transport
\mathrm{O_2}, nutrients, enzymes, hormones ⟶ tissues
\mathrm{CO_2} & metabolic wastes ⟶ excretory organs
Heat distribution → regulation of body temperature
Fluid, electrolyte & pH homeostasis
Protection
Immune surveillance (microbes, foreign Ag, tumors)
Hemostasis → prevents blood loss
Components of the Circulatory System
Cardiovascular system:
heart + blood vessels (arteries, arterioles, capillaries, venules, veins)
Lymphatic system:
returns excess interstitial fluid to venous blood; lymph nodes = immune organs
Composition of Whole Blood
Total volume ≈ 5 L
Two compartments:
Plasma (≈ 55 %)
92 % H₂O, 8 % proteins + solutes (ions, nutrients, gases, wastes)
Serum = Plasma – clotting factors
Formed Elements (≈ 45 %)
\approx 95\% RBCs (erythrocytes) – anucleate
<1\% WBCs (leukocytes) – nucleated
\approx 5\% Platelets (thrombocytes) – anucleate
Hematocrit (Hct)
% RBCs in whole blood
Women: 36\text{–}46\%
Men: 41\text{–}53\%
Example: 80 mL sample → 30 mL RBCs ⇒ \text{Hct}=\frac{30}{80}\times100=37.5\% (within female range)
Plasma Proteins (7–9 % of plasma)
Albumin (60–80 %)
Creates colloid osmotic pressure → draws \mathrm{H_2O} into capillaries, maintains BP & volume
Globulins
Alpha/Beta: lipid carriers
Gamma: antibodies (immunoglobulins)
Fibrinogen → Fibrin
(clotting)
Formed Elements Details
Erythrocytes (RBCs)
Flattened biconcave discs → large SA for diffusion
Lack nuclei & mitochondria; contain ~280 million Hb molecules/RBC
Production rate: \approx 3\times10^{11}\ \text{day}^{-1}
Leukocytes (WBCs)
Have nucleus, mitochondria, amoeboid motility, diapedesis capability
Granular (detox + heparin): neutrophils, eosinophils, basophils
Agranular (phagocytosis/antibodies): lymphocytes, monocytes
Platelets (Thrombocytes)
Smallest, anucleate fragments of megakaryocytes
Majority of clot mass; live 5–9 days
Release serotonin (vasoconstriction) & growth factors for vessel repair
Hematopoiesis
Occurs in myeloid (red marrow) & lymphoid tissue
Output: \approx5\times10^{11} cells/day
Fetal site = liver
Erythropoiesis
Stimulus: renal \mathrm{EPO}
Rate: 2.5\times10^{6}\ \text{sec}^{-1}; lifespan 120 days; old cells removed by liver, spleen, marrow; Fe recycled
Leukopoiesis
Regulated by cytokines (autocrine factors)
Blood Groups & Typing
ABO antigens on RBC membrane
A, B, AB, O (none)
Agglutination / Transfusion Reactions
Type A → anti-B Abs; Type B → anti-A; Type AB → none; Type O → both
Universal donor = O (no antigens); universal recipient = AB (no anti-A/B Abs)
Rh Factor
Rh⁺: D antigen; Rh⁻: none
Erythroblastosis fetalis: Rh⁻ mother sensitized by Rh⁺ fetus → anti-D Abs hemolyze next Rh⁺ fetus
Hemostasis (Bleeding Cessation)
Platelet Plug
(small tears)
Intact endothelium secretes prostacyclin (PGI₂) & NO → inhibit platelet stickiness & vasodilate
Damage exposes collagen;
von Willebrand factor
bridges collagen ↔ platelets
Platelet Release Reaction: ADP, serotonin, thromboxane A₂ (TxA₂)
Serotonin & TxA₂: vasoconstriction; ADP & TxA₂: recruit more platelets → positive feedback until plug forms
Aspirin inhibits TxA₂ synthesis ⇒ antiplatelet effect
Coagulation (Fibrin Clot)
(large tears)
Intrinsic Pathway
(contact activation)
Negatively charged surface → activates factor XII ⇒ cascade ⇒ factor X (prothrombin activator)
Extrinsic Pathway
(tissue factor)
Tissue thromboplastin (factor III) from damaged tissue directly activates factor X (shortcut)
Common Pathway: \mathrm{Prothrombin\ (II) \xrightarrow{Xa+Ca^{2+}+PL} Thrombin}
\mathrm{Fibrinogen\ (I) \xrightarrow{Thrombin} Fibrin \rightarrow polymer}
Hemophilia:
absence of factor VIII (intrinsic)
Vitamin K–dependent factors; Heparin blocks thrombin
Dissolution:
Factor XII → kallikrein → plasminogen → plasmin → digests fibrin
Anticoagulants:
Ca²⁺ chelators (citrate, EDTA), Heparin (activates antithrombin III), Coumarins (vit K antagonism ↓ Ca²⁺ availability)
Heart Anatomy & Circulations
Four chambers: 2 atria (receive) • 2 ventricles (pump)
Two pumps separated by muscular septum
Fibrous skeleton
(dense CT between atria & ventricles): electrical insulation + valve rings (annuli fibrosi)
Pulmonary circuit:
RV → pulmonary arteries → lungs → pulmonary veins → LA
Systemic circuit:
LV → aorta → tissues → veins → RA
Systemic resistance > pulmonary; LV workload ≈ 5–7× RV ⇒ LV wall 3–4× thicker
Flow rates through both circuits
must be equal
Heart Valves
Atrioventricular (AV):
Right = tricuspid; Left = bicuspid/mitral
Chordae tendineae + papillary muscles prevent prolapse during systole
Semilunar:
Aortic & Pulmonary; open in ventricular systole, close in diastole
Cardiac Cycle (Repeat every heartbeat)
Systole = contraction; Diastole = relaxation
Sequence
Isovolumetric Contraction
: ventricles contract, all valves closed, pressure ↑
Ejection
: when P
{vent}>P
{aorta/pulmon} → semilunars open → stroke volume ejected
Isovolumetric Relaxation
: ventricles relax, semilunars shut (dub), all valves closed
Ventricular Filling
: when P
{atria}>P
{vent} → AV valves open; final filling by atrial systole
Pressures: Systemic ≈ 120/80\ \text{mmHg}; Pulmonary ≈ 25/10
Volumes
End-diastolic (EDV) ("preload")
End-systolic (ESV)
Stroke Volume \mathrm{SV = EDV - ESV}; Example: \mathrm{SV}=80-20=60\,mL; \mathrm{EDV>ESV}
Heart Sounds & Murmurs
"Lub"
(S₁): AV closure just after QRS
"Dub"
(S₂): Semilunar closure at T-wave onset
Murmurs = turbulent flow (valve defects or septal defects)
Mitral stenosis → pulmonary hypertension
Incompetent valves → regurgitation
Septal defects (e.g., patent foramen ovale) ⇒ left→right shunt due to higher LV pressure
Electrical Activity & Conduction
Myocardium
Cardiac muscle cells connected by gap junctions → functional syncytium (atria & ventricles separate via fibrous skeleton)
Pacemaker (SA Node)
Resting V_m=-60\,mV → slow depolarization (pacemaker potential) via
HCN Na⁺ channels
(open on hyperpolarization)
Threshold -40\,mV → \mathrm{Ca^{2+}} influx (L-type) → AP upstroke; repolarization via \mathrm{K^{+}} efflux
Autonomic modulation alters slope of pacemaker potential
Ectopic Pacemakers
AV node, Purkinje, etc., have slower intrinsic rates; suppressed by SA overdrive; take over if SA blocked
Contractile Myocardial AP
RMP -90\,mV; rapid Na⁺ upstroke
Plateau (200–300 ms):
balance of slow Ca²⁺ influx vs K⁺ efflux → prolonged refractory period (prevents tetany)
Conduction Pathway
SA node → atrial myocardium → AV node (delay 0.1 s) → Bundle of His → R/L bundle branches → Purkinje fibers (5 m/s) → ventricular myocardium (contr. starts 0.1–0.2 s after atria)
Excitation–Contraction Coupling
Extracellular Ca²⁺ via L-type channels triggers SR Ca²⁺ release (Ca²⁺-induced Ca²⁺-release); Ca²⁺ binds troponin; relaxation via uptake/outflow pumps
Refractory Period
≈ 300 ms (≈ duration of AP) → heart cannot summate contractions
Electrocardiogram (ECG/EKG)
Surface recording of
electrical
events (not mechanical)
P wave:
atrial depolarization
QRS complex:
ventricular depolarization (+ atrial repolarization)
T wave:
ventricular repolarization
Correlation with sounds: S₁ just after QRS; S₂ at start of T
Structure of Blood Vessels
Tunica interna:
endothelium + basement membrane + elastin
Tunica media:
smooth muscle (thicker in arteries)
Tunica externa:
CT
Only
capillaries
= endothelium only → site of exchange
Arteries
Elastic (conducting): elastin; expand (systole) & recoil (diastole) → dampen pulse pressure
Muscular & arterioles: resistance vessels; greatest pressure drop; precapillary sphincters regulate flow; some arteriovenous anastomoses bypass capillaries
Capillary Types
Continuous: tight; small pores; muscle, lung, adipose
Fenestrated: wide pores; kidneys, endocrine, intestines
Discontinuous (sinusoids): large gaps; liver, spleen, marrow
Veins
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