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Chapter 20: Cardiovascular Physiology
Functions of the Heart
--generating blood pressure
--routing blood: seperates pulmonary and systemic circulations
--ensuring one-way flow of blood
--regulating blood supply: changes in contraction rate and force match blood
delivery to changing metabolic needs
Location of the Heart
--behind rib cage, in cavity: allows for greater protection
--in mediastinum: area from sternum to vertebral column and b/w lungs
--Apex: anteriorly, inferiorly, to the left
--Base: posteriorly, superiorly, to the right
Protective Coverings of the Heart
--Pericardium: holds heart in place
*Fibrous: dense irregular CT (tough), protects and anchors the heart,
PREVENTS OVERSTRETCHING
*Serous: thin, delicate membrane
a. Parietal
b. Pericardial Cavity: filled with pericardial fluid
c. Visceral/Epicardium
Layesr of Cardiac Tissue
--Epicardium: visceral layer of serous peicardium
--Myocardium: cardiac muscle layer is bulk of heart
--Endocardium: chamber lining and valves
Anatomy of the Heart
--Sulci
*coronary sulcus: encircle heart and marks boundary b/w atria and ventricle
*ant. interventricular sulcus: anterior boundary b/w ventricles
*post. interventricular sulcus: posterior boundary b/w ventricles
--Chambers
a. Right atrium
*Vessels that enter: superior vena cava, inferior vena cava, coronary
sinus
*Pectinate muscles: on anterior wall
*Fossa ovalis: femnant of fetal foramen oval
*Blood exits via: tricuspid valve
b. Right Ventricle
*Papillary muscles: cone shaped trabeculae carneae (raised bundles of
cardiac muscle)
*Chordae tendineae: cords b/w valve cusps and papillary muscles
(greatest tension during systole, keep AV valves CLOSED)
*Blood leaves through pulmonary semilunar valve to PULOMONARY
TRUNK
c. Left Atrium
*Vessels that enter: 4 pulmonary veins (2R and 2L)
*Blood leaves via bicuspid/mitral/left AV valve (2 cusps)
d. Left Ventricle
*chordae tendineae anchor bicuspid valve to papillary muscle
*trabeculae carneae
*Blood leaves via: aortic semilunar valve into ascending aorta and
coronary arteries
--Valves
*AV Valves
a. OPEN: when ventricular pressure is LOWER than atrial pressure,
ventricles are RELAXED, chordae tendineae are slack, papillary
muscles relaxed
b. CLOSE: when ventricles CONTRACT, chordae tendinae pulled taut,
papillary muscles contract to pull cords and prevent cusps from
everting, prevent backflow of blood into atria
*Semilunar Valves
a. OPEN: ventricular CONTRACTION, allow blood flow into pulmonary
trunk and aorta
b. CLOSE: ventricular RELAXATION: prevents blood from returning to
ventricles, blood fills cusps and tightly closes them
--Fibrous Skeleton
a. consists of a plate of fibrous CT b/w atria and ventricles
b. Functions
*fibrous rings around valves to support (support structure for heart
valves)
*serves as electrical insulation b/w atria and ventricles (prevents
direct propagation of APs to ventricles)
*provides site for muscle attachment of cardiac muscle bundles
--Muscular Differences
a. atria vs. ventricles
*atria thinner than ventricles b/c only pump blood to adjacent
ventricle
b. R vs. L ventricles
*Right ventricle thicker than atria but thinner than left ventricle b/c
only pumps blood to lungs
*Left ventricle: thickest wall b/c supplies systemic circulation
Cardiac vs. Skeletal Muscle
Cardiac Muscle
Striated
One nucleus
Intercalated discs/gap junctions (syncytium)
Autorhythmic cells
AP longer duration
Long refractory period (no tetanus or wave
summation)
Ca++ regulates contraction
Short, branching
Similar thick/thin arrangement
No endomysium
More sarcoplasm and mitochondria (only
aerobic)
Larger T-tubules
Less developed SR (more dependent on
extracellular Ca++)
Prolonged delivery of Ca++ to sarcoplasm
(longer contraction time)
Skeletal Muscle
striated
Multinucleated
--AP shorter duration
Short refractory period
Ca++ regulates contraction
Long, no branches
Similar thick/thin arrangement
Endomysium
Less b/c anaerobic and aerobic
Smaller
More intracellular Ca++ storage
--
Myocardial contraction
--Phases (depolarization/plateu/repolarization, which ion channels open/close and when)
a. 1: DEPOLARIZATION, resting membrane potential is -90mV
*FAST Na+ channels open for rapid depolarization (INFLUX) then
close
b. 2: PLATEU PHASE, 250msec
*SLOW Ca++ channels open, let Ca++ enter (INFLUX) from
extracellular and from storage in SR (this channel also
permeable to
Na+), bind to form cross-bridges and tension development
*K+ channels close (no efflux, therefore keep + inside)
c. 3: REPOLARIZATION, restore resting membrane potential to -90mV
*Ca++ channels CLOSE (EFFLUX)
*K+ channels OPEN
d. 4: REFRACTORY PERIOD
**all ions move via diffusion INC./DEC. IN PERMEABILITY OF IONS
--AP Ventricles vs. AP SA node
a. SA Node AP
*RMP: -60mV (closer to threshold therefore pacemaker b/c reaches
the threshold the fastest)
*prepotential: due to leaky Na+ channels (more channels = increased
slope=increased heart rates)//leacky Cl- or K+ channels decrease
HR b/c dec. membrane potential
b. Ventricular AP
*more negative RMP, no prepotential
Electrical System of the Heart
--SA Node: P cells (pacemaker cells) here, autorhythmic cells, cluster in wall of R atrium
*pacemaker rates: 90-100 times/minute
--Atria: AP spreads from SA node across both atria
--AV Node: AP spreads from SA node, transmits signal to bundle of His (slows the
propagation speed)
*pacemaker rates: 40-50 times/minute
*Conduction speed: SLOWEST .5 m/s
*Slowing speed of Conduction of AV node
a. fewer gap juctions
b. smaller diameter fibers
--Bundle of His: connection b/w atria and ventricles
--Left and Right Bundle Branches: from bundle of His
--Purkinje Fibers: from bundle branches
*pacemaker rates: 20-40 times/minute (fibers in ventricles)
*Conduction speed: FASTEST 4 m/s
--Timing of Atrial and Ventricular Excitation
*50msec spreads through both atria and down to AV node
*100msec DELAY at AV node due to smaller diameter fibers (atria can fully
contract before ventricles contract)
*50 msec excitation spreads through both ventricles simultaneously
EKG
--Phases
*P wave: ATRIAL DEPOLARIZATION, Na+ channels open, depolarizes apex to
base
--large P wave: enlargement of atria
--extra P wave:
*P to Q interval: atria completely depolarized, conduction time from atrial to
ventricular excitation (though all fibers)
--longer P-Q: scarring or coronary heart disease
*QRS complex: VENTRICULAR DEPOLARIZATION, atrial repolarization (c/n
see b/c overpowered by venricular depolarization)
--Enlarged Q: myocardial infarction
--Enlarged R: enlarged ventricles
*S to T interval: ventricles completely depolarized, the PLATEAU
--elevated S-T: above baseline, acute myocardial infarction
--depressed S-T: below baseline, ischemia
*T wave: VENTRICULAR REPOLARIZATION, begins from epicardium to
endocardium from base toward apex
--flatter T: ischemia, coronary disease
--elevated T: kyperkalemia
*Q to T interval: from beginning of ventricular depolarization to end of
ventricular repolarization
--lengthened: due to conduction abnormalities, ischemia, or
myocardial infarction
--Ectopic Pacemakers
a. Atrial Flutter: single ectopic pacemaker (least bad)
*Extra P wave
b. Atrial Fibrillation: no atrial contraction/atrial waves, multiple ectopic
centers
*no clear P wave b/c of random firing
c. Ventricular Flutter
*multiple QRS complexes
d. Ventricular Fibrillation
*no QRS complexes, no uniform contraction, most dangerous
Leads
--Lead connections
*1: from right to left hand
*2: from right hand to left foot
*3: from left foot to left hand
**normal memvement from right to left at about 60 degrees
--Einthoven’s Law
*lead I + lead II = lead III
*used to measure electrical axis of the heart  provides info on heart
position, hypertrophy of ventricles (related to hypertension,
systemic or
pulmonary), bundle branch block (axis deviation towards side of
bundle
block)
--Mean electrical axis of the heart (GUYTON?)
*left deviations/causes
*right deviations/causes
Cardiac Cycle
--Definitions
a. Systole: contraction
b. dicrotic notch: dip in BP when semilunar valves close
c. Diastole: relaxation
d. End diastolic volume (EDV): volume in ventricle at end of diastole, 130mL
e. End systolic volume (ESV): volum in ventricle at end of systole, 60mL
f. Stroke volume (SV): SV = EDV – ESV
*volume of blood ejected/beat from each ventricle, 70mL
g. Ejection fraction: stroke volume as a % of EDV (SV/EDV x 100), 65% of
EDV
*when below 35% = leading cause of sudden cardiac arrect
(defibrillator)
--Phases of Cardiac Cycle
a. Diastole =RELAXATION
*isovolumetric relaxation: brief period when volume in ventricles d/n
change, pressure drops (as ventricles relax) leads to AV valve
opening
*Passive Ventricular Filling (T-P): rapid ventricular filling (blood
flows from full atria)
--Diastasis: blood flows from atria in smaller volume
*Active Ventricular Filling (P-QRS): atrial systole pushes final
2025mL of blood into ventricles
b. Systole = CONTRACTION
*isovolumetric contraction: brief, AV vlaves cose before SL valves
open
*Ventricular ejection: as SL valves open and blood is ejected
--Ventricular Pressures
*blood pressure in aorta 120 mmHg
*blood pressure pulmonary trunk 30mmHg
*difference in ventricle wall thickness allows heart to push SAME AMOUNT of
blood with more force from the left ventricle
--Heart Sounds
a. 1st: “lubb”, AV valves and surrounding fluid vibrations as valves CLOSE at
BEGINNING of ventricular SYSTOLE
b. 2nd: “dupp”, closing of semilunar valves at BEGINNING of ventricular
DIASTOLE, lasts longer
c. 3rd : passive ventricular filling, caused by turbulent blood flow, detected
near end of first 1/3 of diastole, normal in children no usual in adults, may
be a sign of volume overload (congestive heart failure)
d. S4: caused by active ventricular filling (P wave), not audible in normal
adults
*Due to closing of valves
*Listen at: end of chambers or at great vessels
--Heart Murmurs
a. aortic stenosis: abnormally LONG S1/semilunar valve during systole
b. aortic prolapse/regurgitation: long S2/semilunar valve during diastole
c. mitral stenosis: abnormal S2/AV valve during diastole
d. mitral prolapse: small, abnormal S1/AV valve during systole
Volume/Pressure Curve
--Preload: stretch to fill, ventricles filling, AV valve open, from end systolic volume to
end diastolic volume
--Afterload: force need to overcome to open the semilunar valves (systemic bp)
ejection of blood at “b”, semilunar valves open
--systolic vs diastolic insufficiencies
a. systemic hypertension: increased afterload, decreased stroke volume
b. increased contractility: increased stroke volume, more blood pumped,
increased sympathetics
c. increase/decrease in preload
d. vasoconstriction: increased volume to the heart, increased ventricular
filling, increased preload, increased stroke volume
Frank-Starling’s Law of the Heart
--Stroke Volume: SV = EDV – ESV
--Cardiac Output: CO = SV x HR
*at 70mL SV x 75 bpm = 5 ¼ liter/min
*cardiac reserve: maximum output/output at rest
--Mean arterial blood pressure: MAP = CO x TPR
*PR: totally resistance against which blood must be pumped
Control of Blood Pressure, Heart Rate, Contractility
--Cardiovascular system:
*located in medullar oblongata
*sympathetic: increased heart rate and force of contraction, supplied by
cardiac nerves, epinephrine and norepinephrine released
*parasympathetic: decreased heart rate, supplied by vagus nerve,
acetylcholne secreted
--Intrinsic Factors (20-104)
influences of stroke volume: preload
*Frank-Sterling’s Law: volume of the blood ejected by ventricle depends on
volume present in the ventricle at end of diastole
*the more the muscle is stretched the greater the force of contraction
*more blood in ventricles leads to greater force of ventricular contraction
*CARDIAC OUTPUT MUST EQUAL VENOUS RETURN
influences on stroke volume: afterload
*amount of pressure created by blood in arteries
*high blood pressure creates high afterload
influences on stroke volume: contractility
*autonomic nerves, hormones, Ca++ or K+ levels
--Baroreceptors
*Found in: arch of aorta and carotid arteries
*Pathway: inc. BP  detected by baroreceptors  message to CV sytem 
inc parasympathetic stimulation, dec. sympathetic stimulation  dec.
heart
rate and stroke volume  dec. release of epi and norepi  BP decreased
b/c of decreased CO (from Dec. SV and HR)
*Function: control of BP, detect change in BP and send info to CV center
--Hormonal Influences
*Epinephrine: increase HR
*Noreepinephrine: increase HR
*thyroid hormones: increase HR
--Local Factors
*pH/CO2: inc. in CO2 leads to inc. [H+] therefore dec. pH
*O2
--Chemoreceptors: monitor blood chemistry
*Found in: aorta body and carotid body
*Pathway: blood pH dec. (due to inc. in blood CO2)  dec. parasympathetic,
increased sympathetic  inc. heart rate and SV  inc. in blood pH due
to
inc. blood flow to lungs (dec. levels of CO2)
--Ionic Effects on Heart Rate
*Na+
--hypernatremia: elevated Na+, depresses the heart, due to competition of
Na+ with Ca++, prevents Ca++ from carrying out contractile role
*K+
--hyperkalemia: elevated K+, slows heart rate, heart dilates and becomes
flaccid, produces general WEAKNESS of the heart due to dec. in
concentration gradient  less negative membrane potential  dec. in
magnitude of APs  dec. in contraction strength
*Ca++
--hypercalcemia: elevated Ca++, excites the heart, produces bigorous and
prolonged contraction