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2) Gives overall cardiac muscular electric activities (but not specific portion only)
3) Electrocardiogram leads placement (Fig.12-15, Einthoven's triangle)
Each lead is a set of positive and negative electrode (Table 12-2)
Lead I: Right arm(-) and Left arm(+)
Lead II: Right arm(-) and Left leg(+)
Lead III: Left arm(-) and Left leg(+)
4) Paper speed is 25mm/ sec.
Thin vertical line - 0.04sec.
Every fifth heavier line -0.2sec.
5) Heart beat and waves (Fig.12-14, Tracer; conduct)
(1) P wave: Depolarization of the atrial walls -atrial systole
(2) QRS complex: Ventricular depolarization and atrial repolarization -ventricular systole
and atrial diastole
Atrial repolarization is masked by QRS complex
(3) T wave: Ventricular repolarization -ventricular diastole
Length of time during and between the waves indicates the efficiency of conduction
6) Interpretation of electrocardiogram (Fig. 12-16)
P wave: atrial disorders -flutter, fibrillation
QRS wave: ventricular disorders
P-R interval: SA node - AV node block
ST segment: infarction
4. Cardiac muscle contraction
Similar to skeletal muscle contraction with some differences
Sequence of cardiac muscle contraction (Fig. 12-17)
Impulse to sarcolemma
Opening of Ca++ channels (voltage-gated) on T-tubule
Release Ca++ into cytoplasm
Ca++ binds to receptors on the membrane of sarcoplasmic reticulum
Ca++-receptor binding opens receptor integrated Ca++ channels on sarcoplasmic reticulum
Ca++ released from sarcoplasmic reticulum
Ca++ binds to troponin
Intensity of muscle contraction is based on Ca++ concentration in cytoplasm
No tetanic contraction (Fig. 12-18)
-Long refractory period by prolonged plateau of action potential
5. Mechanical events of the cardiac cycle (Fig.12-19a,b)
1) Systole: ventricular contraction and blood ejection
Isovolumetric ventricular contraction
-All valves closed
Ventricular ejection
-AV valve closed
-Aortic and pulmonary valve open
2) Diastole: Ventricular relaxation and blood filling
Isovolumetric ventricular relaxation
-All valves closed
Ventricular filling
-AV valve open
C. Reactive hyperemia
-Monitored by obstruction of arterioles
D. Response to injury
(2) Extrinsic controls
A. Sympathetic nerves
-Norepinephrine: vasoconstriction
B. Parasympathetic nerves
-No innervation
C. Noncholinergic, nonadrenergic autonomic neurons
-Nitric oxide: vasodilator
D. Hormones
-Epinephrine (Fig.12-35)
b -adrenergic receptor vasodilation
a -adrenergic receptor vasoconstriction
-Angiotensin II (kidney): vasoconstriction
-ADH: vasoconstriction
*Summary of controlling factors (Fig.12-36; Fig.12-51)
(3) Arteriolar control in specific organs (Table 12-5a,b)
3) Capillaries
(1) Velocity of capillary blood flow (Fig.12-39)
(2) Movement across capillary wall
Structure of capillary (Fig.12-37)
Through intercellular cleft and fused-vesicle channels
Microcirculation (Fig.12-38)
Exocytosis and endocytosis for larger molecules
Diffusion across capillary wall (Fig.12-40)
Bulk flow across capillary wall (Fig.12-41)
-Filtration of protein-free plasma to interstitial fluid
(3) Factors determining fluid movement across capillaries (Fig.12-42)
Capillary hydrostatic pressure
Interstitial fluid hydrostatic pressure
Osmotic force due to plasma protein concentration
Osmotic force due to interstitial fluid protein concentration
4) Veins
(1) Determinants of venous pressure (Fig.12-46)
Sympathetic neurons: vasocontraction
Relationship between vasoconstriction and vasodilation on blood pressure (Fig.12-43)
Skeletal muscle pump: muscular contraction decreases venous diameter
*peripheral-vein valve (Fig. 12-45)
Respiratory pump: inspiration increases pressure of abdominal veins (through
diaphragm) and decreases pressure of intrathoracic veins and right atrium
5) Lymph vessels
Connect interstitial fluid to cardiovascular system (Fig.12-47)
Joins into the veins near the junction between jugular and subclavian veins
Circulation forces from,
-Contraction of lymphatic organs