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Chapter 12 Cardiovascular physiology

Section A. Overall design of the circulatory system

1. Three components (Table 12-1)
(1) Heart
(2) Blood (Fig.12-1)
Formed elements
RBC (hematocrit)
*Buffy coat
(3) Blood vessels
*Portal vessels
2. Blood circulation
-Systemic and pulmonary circulation (Fig.12-2)
(1) Systemic circulation
Transports blood to and from the body
Left ventricle to right atrium
(2) Pulmonary circulation
Carries blood to and from the lungs
Right ventricle to left atrium
3. Distribution of systemic blood flow in different organs (Fig.12-3)
* Distribution of total blood volume in different parts of cardiovascular system (Fig.12-44)
4. Pressure, flow, and resistance
F = DP/R (Fig.12-4)
F: Blood flow rate
DP: Pressure difference
R: Resistance
R = 8Lh /p r4 (Fig.12-5)
h : Fluid viscosity
L: Length of the tube
r: inside radius of the tube
8/p : constant
(1) Blood viscosity
Hematocrit is a factor
Relatively constant
(2) Length of blood vessels is constant
(3) Inside radius of the blood vessels is resistance determinant

Section B. The Heart

1. Anatomy of heart
1) Lies near the anterior chest wall, directly behind the sternum
2) Surrounded by pericardial cavity (Pericardium)
-Two membranous coverings: pericardium and epicardium
3) Cardiac muscle (Fig.12-9, muscles)
(1) Striated voluntary muscle
(2) Aerobic metabolism: rich in mitochondria and blood vessels
(3) Intercalated disc: cell to cell connection by desmosome junction
(4) Mechanically, chemically, and electrically connected by gap junction
(5) Conducting system
Pacemaker cells
Connected by gap junction
(6) Atrial natriuretic hormone: Decrease blood pressure through Na+ excretion from kidney
4) Blood supply to the heart
(1) Coronary arteries
Left and right coronary arteries
Branch from the base of the aorta
The highest blood pressure in the systemic circuit
(2) Coronary sinus
Large, thin-walled vein
Opens into right atrium below the inferior vena cava
5) Autonomic innervation
Parasympathetic nerve - acetylcholine: decreases heart beat
Sympathetic nerve -norepinephrine: increases heart beat
6) Anatomy and blood flow (Fig.12-6; Heart; Heart anatomy)
(1) Right atrium
Receives blood from the systemic circuit through two large veins
Superior vena cava: blood from the head, neck, upper limbs, and chest
Inferior vena cava: blood from rest of trunk, viscera, and lower limbs
Coronary sinus opens into right atrium, right below the inferior vena cava
- blood from cardiac vein
(2) Right atrioventricular valve (tricuspid valve)
Each cusp is connected through chordae tendineae to papillary muscles
- Limits the movement of valve and proper function (blocking regurgitation)
(3) Right ventricle
Blood from right atrium
Discharges blood into the pulmonary circulation
:Pulmonary trunk branches into right and left pulmonary arteries (venous blood)
Pulmonary semilunar valve between right ventricle and pulmonary trunk
Relatively thin wall
(4) Left atrium
Collects blood from the pulmonary circuit
Blood from right and left pulmonary (superior and inferior) veins (arterial blood)
(5) Left atrioventricular valve (bicuspid valve: mitre)
Each cusp is connected to chordae tendineae to papillary muscles

*Mitral valve prolapse (cuspids)

(6) Left ventricle
Ejects blood into the systemic circuit
Aortic semilunar valve between left ventricle and aorta
Has a thick muscular wall to push blood to the body system
- Need 6 to 7 times more pressure than right ventricle
*Path of blood flow (Fig.12-8 ; Heart circulation)
2. Heartbeat coordination
1) Sequence of excitation (Fig.12-10, Fig.12-11)
(1) Sinoatrial (SA) node
Location: posterior wall of right atrium: "cardiac pacemaker"
Leads contraction of both atria
Determines heart rate
(2) Atrioventricular (AV) node
Location: floor of right atrium
Slow in action potential propagation -provide complete atrial contraction before
ventricular contraction
(3) AV bundle (Bundle of His)
Location: top of interventricular septum
Only electrical link between atrium and ventricle
(4) Right and left bundle
Location: Ventricular septum
(5) Purkinje fibers
Location: contractile cells of the ventricular myocardium
Contraction of ventricle from apex
2) Ventricular action potential (Fig.12-12)
Similar to skeletal muscles or nerve except,
-Maintained plateau status of action potential (caused by K+ and Ca++ channels)
-Decreased potassium permeability after action potential begins
-Increased and prolonged calcium permeability (L-type Ca++ channels)
*L: 'long-lasting'
3) Pacemaker potential at SA node (Fig.12-13)
Responsible for automaticity
Summation of graded potential -gradual depolarization
Involved ion channels;
(1) K+ channels: slow closure after previous action potential
(2) Atrial Na+ channels (designated as f): opens on negative potential
(3) T-type Ca++ channels: transiently opens
(4) L-type Ca++ channels: final boost of depolarization
Inherent rate of SA node is 100 depolarizations per min.
4) Bundle of His has pacemaker cells
Produce pacemaker potentials where AV conduction disorder is present
Slower rate than atrium
3. Electrocardiogram (ECG)
1) Graphic representation of electrical activity generated by the heart
-Measurement of currents at extracellular fluid

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

-Aortic and pulmonary valve closed

-Atrial contraction (at the end of diastole)
3) Pulmonary circulation pressure (Fig.12-21)
3) Summary of cardiac cycle (Fig.12-20)
4) Stroke volume
Stroke volume = End-diastolic volume - End-systolic volume
Stroke volumes of right and left ventricle are the same
6. Heart sounds
"Lub" sound
-Closure of the AV valve at the onset of systole
-Soft and low pitched
"Dup" sound
-Closure of the aortic and pulmonary valves at the onset of diastole
Heart murmurs (Fig.12-22)
-Stenosis (narrowed valves)
-Insufficiency (leaky valves): Prolapsed mitral valve
-Septal defect: Hole in the interventricular septum
7. Cardiac output
1) Cardiac output (CO: L/min) = Heart rate (HR: beats/min) X Stroke volume (SV: L/beat)
Normal: about 5L/min
2) Control of heart rate (Fig.12-24)
(1) Sympathetic nerves: Increase heart rate by shortening time to reach threshold level
of pacemaker potential (Fig.12-23)
Norepinephrine -opens Na+ channels
(2) Parasympathetic nerves: Decrease heart rate; In charge during resting period
Acetylcholine -closes Na+ channels
(3) Hormones: Epinephrine (Adrenal medulla): Increase heart rate
(4) Temperature
(5) Plasma electrolytes
(6) Chemicals
3) Control of stroke volume (stroke volume control)
(1) Contractibility of ventricles
-Frank-Starling mechanism (Starling's law of the heart)
A length-tension relationship
Increase in ventricular end-diastolic volume increases stroke volume (Fig.12-25)
Positive relationship between venous return and cardiac output
-Tension increases by stretching
Provides increased stroke volume
-Ejection fraction (EF)
Measure of contractibility
SV: Stroke volume
EDV: End-diastolic volume
Normal: 50 to 70% under resting condition
(2) Sympathetic input
Higher norepinephrine causes higher ventricular contractility (Fig.12-27)

Stimulation causes increased stroke volume (Fig.12-26)

Stimulation increases availability of Ca++
-Opening of calcium channels on sarcolemma
-Increases calcium absorption into sarcoplasmic reticulum
-Enhances calcium binding to troponin
Effects of autonomic nerves on the heart (Table 12-3)
(3) Afterload (afterload)
Tension produced by ventricle in order to contract
Afterload is increased when,
:aortic pressure is increased
:systemic vascular resistance is increased from aortic valve stenosis
Increased afterload increases end-systolic volume and decreases stroke volume
4) Summary (Fig.12-28)
Section C. Vascular System
1. Endothelial cells
Inner lining of blood vessels
Functions (Table 12-4)
2. Blood pressures (Fig.12-29)
1) Arteries
(1) Compliance: stretchability (Fig.12-30)
Compliance = D volume/D pressure
(2) Arterial pressure (Fig.12-31)
Systolic pressure: at the peak of ventricular ejection
Diastolic pressure: right before the ventricular ejection
Pulse pressure: diastolic pressure systolic pressure
*Factors involved on pulse pressure
-Stroke volume
-Speed of ejection
-Arterial compliance
(3) Measurement of systemic arterial pressure (Fig.12-32)
From brachial artery
Korotkoffs sound
2) Arterioles (Fig.12-33)
- Control of blood flow in arterioles
(1) Local controls
- By dilation or constriction of arterioles
A. Active hyperemia (Fig.12-34a)
- Monitored by metabolic activities
Decreased O2
Increased CO2
Increased hydrogen ion (low pH)
Increased K+
Increased osmolarity
B. Autoregulation (Fig.12-34b)
- Monitored by arterial pressure changes

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

-Contraction of smooth muscle at lymph vessels

-Skeletal muscle contraction
-Respiratory movement
Section D. Regulation of systemic arterial pressure
-Systemic arterial pressure (Fig.12-51)
Mean systemic arterial pressure = Cardiac output X Total peripheral resistance
Blood volume and arterial pressure (Fig.12-52)
1) Baroreceptor reflexes
Monitor changes in blood pressure
Baroreceptor action potential and mean arterial pressure (Fig.12-54)
Arterial pressure control through baroreceptor (Fig.12-55)
Blood pressure compensation by arterial baroreceptor reflex (Fig.12-56)
(1) Arterial baroreceptors (Fig.12-53)
Carotid sinus baroreceptors (neck)
Aortic arch baroreceptor
(2) Medullary cardiovascular center
In medulla oblongata
Receives input through baroreceptors
Innervated into sympathetic and parasympathetic neurons to heart and vessels
(3) Other baroreceptors
Baroreceptors on systemic veins, pulmonary vessels, and walls of heart
2) Arterial pressure and blood volume
Long-term regulation of arterial pressure through blood volume
Increased arterial pressure increases excretion of sodium and water through kidney (Fig.12-57a)
Increased blood volume increases arterial pressure (Fig.12-57b)
3) Other cardiovascular reflexes and responses
Blood concentration of oxygen and carbon dioxide
Blood flow to brain
Pain originating from skin increases arterial pressure (contrast to pain from viscera)
Activities: meeting (up 20mmHg), walking (up 10mmHg), sleeping (down 10mmHg)