Bio 169 Cardiovascular System Study Guide
Spring Semester 2005
Learning Objectives, Topics, Key Words
Readings: Martini, Chapters 20 and 21
1. Understand the general plan of the circulatory system
heart (two pumps side by side) + two flow circuits
pulmonary circuit (to/from lungs)
systemic circuit (to/from the rest of the body)
arteries (away from heart)
capillaries (tissue exchange)
veins (toward heart)
2. Know the gross anatomy of heart and how blood flows through it
in mediastinum
between lungs, sternum, vertebrae
tilted to left
most of heart is to the left of midline
base (right second intercostal space)
atria
apex (left fifth intercostal space)
ventricles
pericardium
double-walled sac
attached to aorta and superior vena cava (the "great vessels") and diaphragm
two serous layers face pericardial cavity
pericardial cavity
pericardial fluid (~30 ml)
fibrous layer on outside of pericardium
function: isolates, protects, limits expansion of heart
pathology:
excess fluid builds up in pericardial cavity --> cardiac tamponade
heart wall (3 layers)
epicardium (= visceral layer of pericardium)
simple squamous epithelium
smooth --> minimize friction
myocardium (= heart muscle)
cardiac myocytes (see Fig 20-5)
short (~ 15 x 200 µm)
branching
striated
mechanically and electrically coupled (at the intercalated discs)
desmosomes (for mechanical coupling)
gap junctions (for electrical coupling, permits intracellular spread of ionic current)
--> atria or ventricles contract as unit
endocardium
simple squamous epithelium (continuous with endothelium of blood vessels)
--> continuous sheet lines the entire CV system -- the layer in contact with blood
heart chambers (4 = 2 atria + 2 ventricles)
atria R and L (singular, atrium)
thin walled
chamber extends in atrial appendages (also called, auricles)
ventricles R and L
R thinner wall (low pressure pump)
L thicker wall (high pressure pump)
since work = pressure x volume, therefor much more work by left ventricle
"cardiac skeleton" connective tissue which attaches atria to ventricles
electrical isolation of atria from ventricles
support atrioventricular (AV) valves
coronary sulcus (a furrow between atria and ventricles)
interatrial septum
fossa ovalis (remnant of foramen ovale in fetus, blood flow skips lungs)
newborn may have atrial septal defect
another skip of lungs in fetal circulation: ductus arterious connects pulmonary trunk to aorta
remnant is ligamentum arteriosum left after ductus closes after birth
newborn may have patent ductus arteriosus
interventricular septum
trabeculae carneae (strands of myocardium projecting from walls of ventricles)
path of blood flow
superior and inferior vena cavae (return from systemic circuit)
right atrium
right ventricle
pulmonary trunk
R and L pulmonary arteries (to pulmonary circuit)
pulmonary veins (from pulmonary circuit
left atrium
left ventricle
aorta (to systemic circulation)
ascending
arch
descending
thoracic
abdominal
heart valves
ensure one-way flow
made of dense connective tissue covered with endothelium
enables CPR effect
atrioventricular (AV) valves
(called, cuspid valves; cusp = point)beween atrium and ventricle
anchored by chordae tendineae to papillary muscles
tricuspid valve on right
mitral (also, bicuspid) valve on left
semilunar valves
(leaflets are half-moon shaped)between ventricle and outflow vessel
pulmonic valve on right
aortic valve on left
pathology (both makes heart work harder)
valvular stenosis (narrowing -- restricts flow)
valvular insufficiency (also, incompetence) (doesnt close ---> permits backward flow)
blood flow to heart
coronary circulation
R and L coronary arteries branch at root of aorta
left anterior descending
circumflex (left chambers)
venous drainage is by coronary veins to coronary sinus (to right atrium)
ischemia
--> angina pectoris (literally, "pain in the breast")
myocardial infarction ("heart attack")
pathololgy: atherosclerotic plaque damages endothelium --> thrombus --> infarction
treatment: thrombolytic agents (e.g, tissue plasminogen activator (t-PA)
emergency coronary arterial bypass graft (CABG - "cabbage")
angioplasty + stent (PTCA, rotorooter)
3. Understand the structure and function of the pacemaker and conduction system of the heart
heart is self exciting
pacemaker cells (produce spontaneous regular action potentials)
pacemaker potential (slow spontaneous depolarization to threshold --> AP)
conduction system (modified cardiac myocytes)
SA (sinoatrial) node
higher intrinsic rhythm than AV node --> makes AV node the normal pacemaker
excites cardiac myocytes of atrium
AV (atrioventricular) node (slow conduction delays delay)
lower intrinsic rhythm than SA node
bundle of His (only normal electrical path from atria to ventricles)
R and L bundle branches
Purkinje fibers (large diameter fibers --> rapid conduction of AP to myocardium)
atria then ventricles is normal sequence
conduction problems treated with implanted artificial pacemaker
4. Understand the shape and ionic mechanisms of the ventricular action potential
phase 0 -- resting potential
phase 1 -- fast depolarization - opening of voltage-gated sodium channels
phase 2 -- plateau of depolarization - opening of voltage-gated calcium ion channels
phase 3 -- repolarization - opening of voltage-gated potassium ion channels
long duration (~300 msec)
long refractory period prevents tetanic contraction
propagates from cell to cell through low resistance gap junctions at intercalated disks
5. Know the waves of the electrocardiogram (EKG) and their relation to the cardiac action potentials
bipolar limb leads (difference in potential between two limbs)
P wave (atrial depolarization)
QRS wave (ventricular depolarization, duration is ~0.05 to 0.10 sec)
T wave (ventricular repolarization)
PR interval (mostly AV conduction delay, < 0.2 sec)
QT is called "electrical systole"
ST segment (plateau phase of cardiac action potential)
stress test (treadmill exercise + EKG: look for ischemic changes )
6. Recognize common arrythmias (i.e., not normal sinus rhythm)
normal sinus rhythm
sinus tachycardia
sinus bradycardia
heart blocks (problem in conduction system)
first degree (PR interval > 0.2 sec)
second degree (some Ps not followed by QRSs)
third degree (Ps independent of QRSs)
preventricular contraction (PVCs, VPBs)
caused by an "ectopic focus" -- spontaneous action potentials in ventricular myocardium
skip a beat
paroxysmal tachycardias (caused by rapidly discharging ectopic focus)
atrial fibrillation ("A fib") (leads to blood clot in atrial appendage)
ventricular fibrillation (common in myocardial infarction)
defibrillator shocks cardiac myocytes --> synchronizes AP --> refractory period
7. Understand the events of the cardiac cycle and their causal interrelationships
Hint: use the EKG to understand the mechanical events (pressure, flow, valve action)
overview:
systole - contracting phase
contraction initiated by depolarization of atrial and ventricular myocytes
both atria first, then both ventricles
blood pushed into ventricles by atria
blood ejected into aorta and pulmonary trunk
diastole - resting phase
relaxation initiated by repolarization of cardiac myocytes
chambers refill during their diastole
atria
atrial diastole
fill as blood returns from vena cavae and pulmonary veins
flows into ventricles through open AV valves
atrial systole
P wave
atria contract and push more blood into ventricles
ventricles
ventricular systole
QRS complex
ventricles contract
pressure rises
AV valves close, semilunar valves open
ejection phase
starts when semilunar valves open
ends when semilunar valves close
end systolic volume (ESV, ~60 ml)
ventricular diastole
T wave
ventricular pressure drops
semilunar valves close
aortic pressure drops as blood flows into circulation
ventricular filling
AV valves open - filling begins
atrial contraction sends in a bit more blood
end diastolic volume (~130 ml) (EDV)
stroke volume (SV = EDV - ESV)
ejection fraction = fraction of diastolic volume ejected during systole
ejection fraction SV/EDV, e.g. 70ml/130 ml = 0.54)
heart sounds
caused by turbulent flow as valves close
S1 - lubb
closing of AV valves
S2 - dup
closing of semilunar valves
heard best over particular spots on chest (with stethoscope)
murmurs two possible causes
stenosis - narrowing leads to turbulent flow
insufficiency - partially open valve leads to turbulent flow
8. Understand cardiac output and the factors that influence it
equation: CO = SV x HR
in words: cardiac output equals stroke volume times heart rate
cardiac output - outflow from heart in L/min
R and L flows are equal
stroke volume - outflow per beat (L/beat)
EDV - ESV
heart rate - beats/min
L/beat x beats/min = L/min
e.g., 0.07 liters x 75 beats/min = 5.3 liters/minute
3 factors affecting stroke volume (SV)
"preload" (actually, end diastolic volume, EDV)
stretch of resting myocytes increases resting sarcomere length
Starlings "Law of the Heart" (SV goes up as EDV goes up)
"contractility" (a measure of the power of the myocardium)
increased by sympathetic input to myocardium
positive and negative inotropic effects (affects ejection fraction)
caused partly by changes in Ca2+ released from sarcoplasmic reticulum
"afterload" increased by:
elevated diastolic aortic pressure, or
increased vascular resistance (due to constiction of blood vessels), or
aortic stenosis
control of heart rate (HR)
two autonomic inputs to SA node
vagus (CN X)-- slows down
cardioaccelator nerves -- speeds up
neurotransmitter affects slope of pacemaker potential
acetylcholine -- slower depolarization
norepinephrine -- faster depolarization
9. Understand the anatomy of the blood vessels
overview:
closed circuit of tubes
heart --> arteries -->
arterioles -->
microcirculation -->
venules -->
veins --> heart
arteries
lumen + 3 tunics
tunica interna (intima)
endothelium (simple squamous)
basement membrane
internal elastic lamina
elastic fibers -- store and release energy
made of elastin
tunica media (media)
smooth muscle
wraps around circumference
relax --> vasodilation
contract --> vasoconstriction
external elastic lamina
tunic externa (adventitia)
connective tissue
grades off into surrounding tissue
no epithelium
elastic arteries (large)
act as pressure reservoir -- stretch in systole, recoil in diastole
muscular arteries (medium size)
arterioles (very small arteries)
thick wall (media) compared to lumen
main control of peripheral resistance and therefor, blood flow
microcirculation
metarterioles
precapillary sphinchter
vasomotion
control by tissue metabolites
nitric oxide from endothelium
capillaries
continuous (or, true) capillaries
fenestrated capillaries (especially in endocrine organs)
sinusoids (in liver, spleen)
thoroughfare channel (bypass the capillaries)
venules
no smooth muscle
veins
valves keep flow going toward heart
blood distribution
veins >60%
other <40%
10. Understand hemodynamics (physiology of the circulation)
pressure drives flow (flow in liters/min)
flow = pressure drop/resistance (law of bulk flow of fluids in a tube)
blood pressure drops from arteries to veins
control of resistance
up with viscosity (effect of hematocrit)
up as vessel length goes up (growth or obesity)
down as vessel radius goes up (biggest effect: goes as fourth power of the radius!)
total peripheral resistance (TPR) (also, systemic vascular resistance, SVR)
capillary exchange
diffusion (from high to low concentration; e.g., glucose from blood to cells)
lymph formation
filtration and resorption of water (Starlings principle of the capillaries)
outward forces:
blood hydrostatic pressure (BHP)
interstitial fluid osmotic pressure (IFOP)
inward forces:
blood colloid osmotic pressure (BCOP) (colloid = proteins such as albumin)
interstitial fluid hydrostatic pressure (IFHP)
net filtration pressure (NFP)
= (sum of forces pushing fluid out) - (sum of forces pulling fluid in)
NFP = (BHP + IFOP) - (BCOP + IFHP)
NFP at arteriole end is higher than NFP at venule end --> fluid (3.6 liters/day) leaves the capillaries as lymph!
lymph vessels
carry lymph back to heart and filter through the lymph nodes
edema
= accumulation of fluid in tissues
therapies:
compression bandage (increase IFHP)
elevation (decrease BHP)
increase protein intake (increase BCOP)
factors affecting venous return
(venous return must equal cardiac output, VR = CO)right atrial pressure
(elevated PRA lowers VR) because:
mean systemic filling pressure (think of vessels like balloon filled with blood)
blood volume affects it directly
volume of venous reservoir
smooth muscle contraction in media controls size of venous reservoir
12. Understand the mechanisms that control and regulate blood pressure
the plumbing basics:
recall: flow = pressure drop/resistance (law of bulk flow of fluids in a tube)
CO = MABP/TPR (specific form for circulation; MABP is mean arterial blood pressure)
neural control of cardiovascular system
inputs
peripheral receptors
baroreceptors (sense BP in aortic arch, carotid artery)
chemoreceptors (3 kinds: CO2, O2, pH)
higher centers (e.g., emotions, thermoregulatory, experience)
integration
cardiovascular neurons scattered in medulla
vasomotor center
vasoconstrictor
vasodilator
outputs (ANS)
heart rate: vagus nerve, cardioaccelerator nerve to SA node
contractility (affects stroke volume): sympathetic input to myocardial cells
nervous control of TPR
affects smooth muscle of blood vessels (arterioles mainly) -->
vasoconstriction or vasodilation
"vasomotor tone"
balance of vasoconstriction/vasodilation controls distribution of CO among organs
sympathetic response depends on type of adrenergic receptor on smooth muscle cells
alpha adrenergic receptors--> vasoconstriction (e.g., in viscera, skin)
beta adrenergic receptors --> vasodilation (e.g., coronaries)
hormonal control of blood pressure
epinephrine: increase heart rate and force --> CO --> incr. BP
antidiuretic hormone (ADH): increase blood volume by retaining water --> incr. BP
renin-angiotensin: two ways to increase BP:
--> aldosterone --> increase blood volume by retaining sodium --> incr. BP
--> vasoconstriction --> incr. TPR --> incr. BP
shock (inadequate cardiac output)
cardiogenic (e.g., myocardial infarction)
hypovolemic (e.g. hemorrhage)
loss of vasomotor tone (e.g., grave trauma)
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Durham Technical Community College
Durham, NC 27703
Last updated 9 February 2005