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Bio 169 Cardiovascular System Study Guide
Spring Semester 2005

Learning Objectives, Topics, Key Words



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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) (doesn’t 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

Starling’s "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 (Starling’s 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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Last updated 9 February 2005