Cardiovascular From FA Organ Systems and Goljan Constance

Embryology
Septa
Formation
Primitive heart tube formed by lateral folding an fusion of endocardial heart tubes. Dilatations adult heart structures.
Atrial Septum: initial division into L and R atria. Septum primum out toward atrioventricular (AV) septum and close the ostium primum
(ostium is latin for hole). Ostium secundum: tissue regresses in the center of the septum primum. Septum secundum from R edge of septum
primum fuses with Septum primum to close the ostium secundum; fusion Atrial septum. There remains a defect in the septum secundum
called the foramen ovale which allows blood to shunt from Right Atrium (RA) to left Atrium (LA). After birth, | pressure in LA close
foramen ovale.
Interventricular (IV) septum: has two parts; a muscular portion and a membranous portion. The muscular IV septum forms upward from
the base of the primitive ventricle toward the AV septum but doesnt reach it, leaving a gap called the interventricular foramen. The
membranous IV septum grows down from the AC cushions, fusing with the muscular septum to obliterate the IV foramen.
Aorticopulmonary (AP) septum: from neural crest cells that migrate into the conotruncal ridges. Separates the truncus arteriosus into the
aorta and the pulmonary trunk. It spirals as it descends so the aorta is the L ventricular outflow tract and the pulmonary trunk is the R
ventricular outflow tract. Spiraling failure congenital malformations.
Septal
Congenital
Malformations
Atrial Septal Defect:
occurs when an opening
in atrial septum allows
blood to flow between
atria; usu ostium
secundum. Usu Asx;
signs are: wide, fixed
splitting of S2; systolic
ejection murmur heard at
2
nd
intercostal space
(ICS) on left sternal
border (LSB)
Ventricular Septal
Defect: An abnormal
opening in the IV septum;
most common congenital
heart malformation. Usu
in membranous septum.
Large VSDs L-R
shunting; can have easy
fatigability, and a harsh
holosystolic murmer at
the Lower LSB.
Persistent Truncus
Arteriosus: abnl
migration of neural crest
cells; no formation of AP
septum common tract
leaving the vessels;
mixed O2/deO2 blood
R-L shunting, early
cyanosis.
Transposition of the
great vessels: failure of
spiral development of AP
septum. L ventricle (LV)
connects to pulmonary
trunk; R ventricle (RV)
connects to aorta. A
complete R-L shunt and
early cyanosis
Tetralogy of Fallot: due
to anterior displacemt of
the AP septum. Get
overriding aorta (RV
outflow obstruction) and
pulmonic stenosis (RV
hypertrophy). Failure of
AP septum fusion with
muscular IV septum
membranous VSD. 4
th

defect is R-L shunting
early cyanosis
Early
Structures
and
Derivatives
Embryonic/Fetal Structure Adult Derivative
Truncus arteriosus Ascending aorta and pulmonary trunk
Bulbus cordis Smooth parts of the L and R ventricles
Primitive ventricle Trabeculated parts of the L and R ventricles
Primitive atrium Trabeculated parts of the L and R atria
Left horn of sinus venosus (SV) Coronary sinus
Right horn of SV Smooth part of R atrium
Right common cardinal vein and right anterior cardinal vein Superior Vena Cava
Umbilical vein Ligamentum teres hepatis
Umbilical areteries Medial umbilical ligaments
Ductus venosus Ligamentum venosum
Ductus arteriosus Ligamentum arteriosus
Aortic Arches Aortic Arch Adult Structure
First Part of the maxillary artery
Second Stapedial artery
Third Common carotid and proximal internal carotid artery
Fourth Aortic arch and proximal part of the R subclavian artery
Fifth Regresses in humans
Sixth Proximal pulmonary arteries and ductus arteriosus
Fetal
Erythropoesis
Organ involvement: RBCs are produced in different locations throughout the life of the fetus.
Yolk Sac: 3-8 weeks; Liver: 6-30 weeks; Spleen: 9-28 weeks; Bone Marrow: 28 weeks-adult
Hemoglobin: Fetal hemoglobin has two o units and two units (instead of | units)
Fetal
Circulation
Deoxygenated blood leaves via umbilical arteries toward the placenta. Oxygenated blood returns from the placenta via the umbilical veins;
bypasses the liver by flowing through the ductus venosus and into the inferior vena cava which then goes to the right atrium. High pressure
in the right heart (vs left); allows to bypass the pulmonary circulation via 2 methods: 1) flow through the foramen ovale to the LA, LV,
aortahead; or 2) RV, pulmonary trunk, ductus arteriosus, aortatrunk and lower limbs. From fetal tissues iliac arteries umbilical
artery placenta. After birth, breathing + pulmonary arterial resistance pressure in left heart >> pressure in right heart; forces septum
primum against septum secundum and foramen ovale closure. Increased O2 falling levels of prostaglandins ductus arteriosus closure.
Arterial
Congenital
Malformations
Coarctation of the aorta: An abnormal narrowing of the aorta in the area surrounding the
ductus arteriosus. Either Preductal/Postductal:
Preductal coarctation: constriction of the aorta proximal to the ductus arteriosus; patent
ductus arteriosus and R-L shunt with enough blood to the lower extremities.
Postductal coarctation: constriction of the aorta distal to the ductus arteriosus; |BP in the arms
and +BP in the legs (weak or absent femoral pulses). Blood flows from the aorta internal
thoracic intercostal arteries superior epigastric external iliac legs. |flow to the
intercostals dilation rib notching.
Patent Ductus Arteriosus: Failure of
the ductus arteriosus to close
persistent connection b/w the L
pulmonary artery and the aortic arch.
Since L heart has higher pressure, L-
R shunt: blood from aorta to pulmonary
artery. Most common in premature
infants; no cyanosis; can give
prostaglandin inhibitors (indomethacin,
NSAIDs) to help close the PDA.

Cardiovascular Embryology
Right to Left
Shunts
Associated with early cyanosis. Can be caused by any of the 5 Ts: Truncus arteriosus; transposition of the great vessels; tetralogy of Fallot;
total anomalous pulmonary venous return (none of pulmonary veins take blood back to heart); and tricuspid atresia (absence). Each leads to
shunting of deoxygenated blood into oxygenated blood which + the partial pressure of O2 and early cyanosis.
Left to Right
Shunts
Associated with late cyanosis. Can be caused by VSD, ASD, and PDA. These lead to high flow through the pulmonary circulation, which
causes the pulmonary arterial system to hypertrophy and become fibrotic. Pulmonary hypertension (PAH) and right ventricular hypertrophy
can develop. When pressure in the right heart begins to exceed pressure in the left heart, the shunt reverses to become R-L. This is called
Eisenmengers syndrome and causes late cyanosis.
Congenital
Defect
Associations
Disorder Cardiac Defect
22q11 Deletions Truncus arteriosus, tetraology of Fallot
Downs syndrome VSD, ASD
Turners syndrome Coarctation of the aorta
Offspring of a diabetic mother Transposition of the great vessels
Anatomy
Surfaces &
Borders
Anterior (sternal) surface: Right ventricle. Posterior: Left atrium, close to the esophagus.
Right: Right atrium; b/w 3
rd
and 6
th
rib on RSB. Left: Left atrium and Left ventricle.: b/w 3
rd
and 6
th
ribs from LSB to mid-clavicular line.
Apex: left ventricle at 5
th
intercostal space (ICS) at the mid-clavicular line; point of maxima impulse (PMI)\
Aortic Arch: at the sternal notch; vertebral level T2.
Superior Vena Cava (SVC): Enters right atrium at the level of the 3
rd
rib.
Heart Layers Endocardium Innermost; contacts the blood; composed of simple squamous epithelium (endothelium) and underlying connective
tissue
Myocardium Middle layer; made of myoctyes: contractile cells responsible for pumping blood through the heart.
Pericardium Covers heart and proximal portion of the great vessels. 2 layers: fibrous and serous (serous has 2 sublayers). Cardiac
tamponade is compression of the heart by fluid in the pericardial sac +CO. Signs: +MAP, distended neck vains,
pulsus paradoxus, and electrical alternans. Need Pericardiocentesis. Pericarditis is inflammation of the pericardium;
associated with SLA, rheumatoid arthritis, MI, TB, and malignancy. Signs: Chest pain, friction rub, diffuse ST elevation.
Fibrous pericardium: tough CT that tethers heart in
place; connect to sternum and central tendon of the
diaphragm
Serous pericardium: Parietal layer connects to internal
fibrous pericardium. Visceral layer (aka epicardium) is thin
outermost layer of the heart and has the major branches
of the coronary arteries.
Coronary
Arteries
Arise from the proximal aorta as the right and left coronary arteries (RCA; LCA). Vessels are just deep to the epicardium; supplies the
epicardium and myocardium. Heart has a dual blood supply since the endocardium receives nutrients directly from contacting the blood.
When coronary artery infarct happens, subendocardial tissue is most damaged b/c farthest from either blood supply; subendocardial
infarcts can result from unstable angina (CA occlusion), severe anemia, or hypotension; see ST segment depression, fibrosis, and
vacuolization. Coronary artery flow happens mainly during diastole b/c myocardial contraction in systole puts too much pressure on the CA.
Tachycardia shortens diastole so the heart gets less blood supply.
Major branches of the LCA: Left anterior descending (LAD) and the left circumflex
artery (LXA). The LAD is most commonly involved in MI infarction of the anterior
portion of the ventricles, cardiac apex, and IVS.
Major branches of the RCA: Marginal artery (RMA)
and posterior descending artery (PDArtery). The
RCA is the second most commonly occluded artery.
Right
dominant
arterial supply
and ECG
findings on MI
Artery LAD Left Circumflex RCA
Location Anterior wall of LV Lateral wall of LV Lateral wall of RV
Areas supplied Anterior wall of LV, Apex, and
Anterior 2/3 of IV septum
Lateral wall of LV, Posterior wall
of LV (20%), posterior 1/3 of IV
septum (20%)
Lateral wall of RV, posterior wall of LV
(80%), Posterior 1/3 of IV septum
(80%); SA node & AV node
Area of infarct Septum Lateral LV wall Inferior RV wall
Leads with ST elevation V2, V3 I, aVL, V5, V6 II, III, aVF
Conduction
system
Sinoatrial Node SA node: the cardiac pacemaker, sets rate (about 7 bpm). Contains specialized myoctyes that depolarize
rhythmically, initiate electrical impulse spread; also gets sympathetic input (|rate) and parasympathetic input
(+rate) from the vagus. Located at the junction of the RA and the SVC just beneath the pericardium; supplied by
the SA nodal artery (usu a branch of the RCA). From the SA atrial spetum LA and AV septum of R heart
AV node
Atrioventricular Node AV node: disperses electrical signals to both ventricles via the bundles of His. In subendocardial CT in
interatrial septum near ostium of the coronary sinus. Blood supply from the AV nodal artery (usu a branch of the
RCA). Damage to AV node (usu from ischemia) complete heart block; slow ventricular rate and +CO.
Bundles of His Travel parallel to the IVS deep to the endocardium, terminate as purkinje fibers in the walls of both ventricles.
Heart Valves Valve Location Structure Auscultate Open Phase
Tricuspid B/w RA and RV Tricuspid Left 5
th
ICS at SB Diastole
Pulmonic B/w RV and pulmonary trunk Semilunar (3 cusps) Right 2
nd
ICS at SB Systole
Mitral B/w LA and LV Bicuspid Left 5
th
ICS at midclavicular line Diastole
Aortic B/w LV and aorta Semilunar (3 cusps) Left 2
nd
ICS at SB Systole




Cardiovascular Anatomy
Major Aortic
Branches
Level Artery Nearby structures Arterial branches Supplies:
T12 Celiac
Trunk
Posterior to gastrohepatic
ligament; superior to stomach
curvature
Common hepatic, splenic, left
gastric arteries
Forgut structures (liver,
gallbladder, stomach, spleen, 1
st

part duodenum)
L1 Superior
Mesenteric
Posterior to neck of pancreas and
stomach antrum
Middle colic, right colic, ileocolic
arteries
Midgut structures (lower duodenum
to splenic flexure of colon;
appendix)
L2 Renal Posterior to renal veins Inferior suprarenal, Segmental
interlobar, arcuate, interlobular
Kidneys, part of suprarenal glands
L3 Inferior
Mesenteric
Posterior to 3
rd
part of duodenum Left colic, sigmoid, superior rectal
arteries
Hindgut structures (splenic flexure
of colon to proximal rectum)
L4 Common
Iliacs
(Aortic bifurcation) Anterior to
formation of IVC
External, internal iliac arteries Pelvis, lower extremities
Physiology
Excitable
Cells
Cardiac nodal cells vs. neurons: both rely on cationic Na+ influx to
reach threshold membrane potential action potentials; but nodal
APs are automatic/spontaneous depolarization.
Cardiac vs. Skeletal myoctes: Both rely on Ca2+ influx for
contraction; but cardiac myocyte AP shape has a plateau due to
inward C2+ current and they have electrical coupling by gap jxns.
Resting
Membrane
Potential
The membrane potential Vm is determined by the relative permeability of certain ions (K+, Na+, Ca2+) and the Relative intracellular and
extracellular concentrations of these ions. Vm is determined by relative contributions of different ion conductances; predominant ion
conductance pushes Vm toward that ions Nerst potential. Ex: At rest, myoctye is more permeable to K+; so Vm is closer to Nernst potential
of K+ than Na+
The resting membrane potential is determined mostly by K+ conductance; [K+]intracellular; and [K+]extracellular. Remember that
[K+]i>>[K+]e and [Na+]e>>[Na+]i. K+ diffuses out of the cell and down the gradient to make Vm more negative (outward current). At a
certain Vm, the net force driving K+ out = force driving K+ in; this is the equilibium potential (aka Nersnt potential):
Vm = 61.51*log ([K+]e / [K+]i) mV
In contrast, Na+ tends to enter the cell and make the Vm more positive (inward current). The Na/K ATPase pump maintains the gradient by
pumping out 3Na+ for every 2K+ that comes in. This keeps the extracellular Na+ > intracellular Na+
Action
Potentials
Two populations of excitable cells; one makes fast-response APs and the other makes slow response APs.
Slow Pacemaker Action Potentials Fast Action Potentials
General SA node; intrinsic pacemaker; highest intrinsic firing rate
(100-120x/m). AV node is latent; can take over if SA is off
(40-60x/m)
His-Purkinje fibers are the tertiary pacemaker cells, after
the SA and AV nodes. Fires at 30-40x/minute.
AP length 150ms (SA, atria), 250ms (AV, ventricles) 100ms
Tissues SA and AV nodes Atria, Ventricles, Purkinje fibers
Antiarrhythmics Class II | Blockers (Phase IV)
Class IV Ca Channel Blockers (Phase 0)
Class Ia, Ib, Ic (Phase 0)
Class III (Phase III)
Upstroke:
Phase 0
Due to slow inwards Ca2+ current through voltage gated
Ca2+ channels; lack fast voltage gated Na+ channels
slow conduction velocity
Due to rapid inward Na+ current through voltage gated
Na+ channels.
1
st
repolarization:
Phase I
Not Present
Inactivation of voltage gated Na+ channels; voltage gated
K+ channels begin to open
Plateau: Phase II Ca2+ influx through voltage gates Ca2_ channels
balances K+ efflux; Ca2+ influx also triggers intracellular
Ca2+ release form sarcoplasmic reticulummyocyte
contraction
Repolarization:
Phase III
Increased K+ conductance K+ efflux Massive K+ efflux due to opening of voltage gated slow
K+ channels and closure of voltage gated Ca2+ channels
Phase IV Slow diastolic depolarization; membrane potential
spontaneously depolarizes as Na+ conductance
increases; accounts for automaticity of SA and AV nodes;
the slope of Phase IV in SA node determines HR
Resting potential; high K+ permeability through K+
channels
Conduction
Velocity
0.01-0.10 per second; slow conduction velocity means
ventricular depolarization is delayed, allowing atria to fully
empty | ventricular filing and CO
0.3-3.0 per second (larger inward current)
Refractory
Period
The period of the AP in which the cardiac cells cannoth be excited; 3 definitions:
Absolute: begins at phase 0 and ends after phase 2; reflects time in which no AP can be generated regardless of inward current
Effective: period in which a conducted AP cannot be generated; slightly longer than absolute
Relative: Period in which an AP can be generated with a larger than usual inward current.
Cardiac
Muscle and
Contraction
When cardiac AP reaches the axon terminal, depolarization of terminal opens vg-Ca2+ channels ACh vesicle fusion and exocytosis. ACh
binds post-synaptic receptor depolarization of the post-synaptic muscle cell. Via Excitation-contraction coupling, the depolarization event
triggers release of intracellular Ca2+ from the sarcoplasmic reticulum (SR). | Ca2+ binds troponin C and changes the conformation of the
myosin-actin complex leading to contraction. Contractiliy generated is related to the intracellular [Ca2+]


Cardiovascular - Physiology
Excitation
Contraction
Coupling
Structures
Sarcomere Contractile unit of myocardial cell that runs from Z line to Z line; Composed of thick filaments (myosin) and
thin filaments (actin, troponin, tropomyosin)
T Tubules Part of the cell membrane that invaginates at the Z line. They carry APs into the cell interior
Sarcoplasmic Reticulum (SR) Intracellular site of storage and release of Ca2+ (used in excitation contraction couplind)
Intercalated Disks Located at the ends of cells. Mediate adhesion between cells.
Gap Junctions Occur at the intercalated disks. Proves a low resistance path for action potentials to spread rapidly
Myocardial
Contraction
and
Relaxation
Cardiac myocyte translates electrical signal into physical response through 4 steps: Extracellular Ca2+ enters cell Ca2+ induces
intracellular Ca2+ release myocardial contraction myocardial relaxation
EC Ca2+ influx AP from cell membrane into Ttubules; during plateau phase, Ca also enters through vg (L-type) Ca2+ channels
Ca2+-induced Ca2+
release
EC Ca Influx is not enough for contraction. EC Ca2+ binds ryanodine receptors (Ca2+ release channels) on the
SR, stimulating more Ca2+ release from the SR. Amount released depends on: 1) size of the inward current during
plateau; and 2) amount of Ca2+ stored in SR.
Myocardial contraction Ca2+ release |concentration; Ca2+ binds troponin C, which causes a conformational change and moves
tropomyosin out of the myosin binding groove on the actin filament. Myosin binds actin; bound myosin head
undergoes shape change to move the thin filament (actin; this is the power stroke) and shorten the sarcomere.
Contraction HIZ shrinkage: H (only thick), I (only thin), and Z band contraction.
Myocardial relaxation Happens when Ca2+ is pumped back into the SR via Ca2+ ATPase. Reduces Ca2+ and removes Ca2+ from
troponin.
Cardiac vs.
Skeletal
Muscle
Cardiac muscle AP has a plateau due to Ca2+ influx; cardiac nodal cells spontaneously depolarize (automaticity); cardiac myocytes are
electrically coupled by gap junctions; cardiac muscle cells have more mitochondria; cardiac muscle increases contractile force by changing
fiber contractility (vs increasing the number of skeletal muscle fibers activated)
Contractility The amount of force cardiac muscle can generate at a given length; related to [Ca2+]i. Can estimate with the ejection fraction (EF):
EF = stroke volume / end-diastolic volume (normal = 55%)
Contractility Increased by Contractility Decreased by:
Increased HR: As HR |, Ca2+ clearance is less efficient intracellular Ca2+ build-up.
Sympathetic stimulation: Stimulation leads to increased Ca2+ influx and | activity of SR
Ca2+ ATPase
Cardiac glycosides (digoxin): inhibit Na/K ATPase in the myocardial cell membrane |
[Na+]I and + Na+ gradient; Since Ca2+ extrusion depends on the Na+ concentration
gradient, less Ca2+ is removed and | [Ca2+]i
|-blockade, Calcium Channel Blockers
Heart Failure
Peripheral nervous system stimulation
Acidosis, hypoxia, and hypercapnia
Preload Refers to the load seen by cardiac myocytes when the heart is relaxeds. Represents the stretch on the filled ventricle during diastole, vefore
contraction takes place. Related to sarcomere length, left ventricular end-diastolic volume (LVEDV), and left ventricular end-diastolic
pressure (LVEDP). An acute | in diastole | force of contraction in systole.
Increases with exercise (a little), increased blood volume (over transfusion) and excitement (sympathetics)
Afterload Load against which myocytes must contract to generate CO. = force needed to push blood from LV to aorta. An acute | + volume
ejected during systole. In the LV, afterload=aortic pressure and MAP/systolic pressure. In the RV, afterload=pulmonary artery pressure and
LVEDV.
Frank Starling
Relationship
| venous return | CO; analogous to: | initial length of muscle in diastole/preload | force of systolic contraction
Molecular/Cellular level: Sarcomere length: proportional to the force of contraction it generates: longer=more cross bridges=more
tension=optimized overlapping of actin-myosin filaments (up to a certain point of stretch)
Organ Level: Increased venous return or end-diastolic volume (preload) | ventricular fiber length and tension |SV and CO. The
frank starling curve can be shifted up in a state of increased contractility; down in decreased contractility.
Caveat: overstretch is possible. Accounts for descending limb of length/tension curve.
Pressure
Volume loops
Describe the relationship b/w LV volume and pressure during the 5 phases of the cardiac cycle: Diastole, with isolvolumetic contraction; then
systole, which systolic ejection, isovolumetric relaxation, rapid filling, and slow filling. Make sure you can draw these!
Diastole Mitral valve (MV) opens, ventricle rapidly fills till pressure of the LV>LA MV closes. Corresponds to P and PR intervals on ECG.
Isovolumetric contraction: Period bw MV closure and Aortic Valve (AoV) opening. Since MV and AoV are closed, the LV is a closed
chamber and must contract under constant volume. Eventually, LV pressure> Aortic pressure AoV opens. Corresponds to QRS on
ECG; the period of highest O2 consumption.
Systole Occures after the AoV has opened: Systolic Ejection: Period between AoV opening and closing. Volume ejected from the LV in this phase
is the stroke volume (SV; also the width of the pressure volume loop). LV pressure + and AoV closes: corresponds to ST on ECG.
Isovolumetric Relaxation: Period b/w AoV closing and MV opening. LV is a closed chamber again, and relaxes until LV pressure drops to
that of the LA MV opens: Corresponds to T wave on ECG
Rapid filling: Period just after MV opening. Slow Filling: Period just before MV closure
Stroke
Volume
Effects
Variable Effect
Increased preload and venous return (ex: aortic insufficiency) |
Increased afterload (ex: HTN, Aortic stenosis) +
Increased contractility (ex: exercise) |
Cardiac vs
Vascular
Function
Cardiac function curve: Aka Frank Starling: |preload/venous return
|CO; + preload/venous return +CO
Vascular Function Curve: | right atrial or systemic pressure
and/or ++ blood volume + venous return/preload; +right
atrial or systemic pressure or || blood volume | venous
return/preload

Cardiovascular - Physiology
Vascular
Function
Curve
NB: The
effects of SVP
dont make
sense to me
FA may be
wrong??
Vascular function curve: blood volume vs preload: | blood volume or + systemic pressure | preload and CO (and vice versa).
Decreased blood volume (hemorrhage, shock) shifts the vascular function curve left and downwards + potential venous return and |
mean systemic pressure through sympathetic stimulation
Exercise: shift the vascular function curve up and right | potential venous return; also | mean systemic pressure through sympathetic
stimulation
X-intercept of vascular function curve=Mean Systemic Pressure: pressure in RA when there is no blood flow through the CV system
Intersection of cardiac and vascular function curve yield equilibrium point: CO=venous return; this is resting CO.
Cardiac
Output
Volume of blood pumped from either ventricle per minute. Normally 4-8L/min and can increase 5-6 times during exercise.
CO=SV*HR
or use Ficks method: can calculate CO by measuring O2 consumption. The amount of O2 delivered to the body is the product of CO and
the difference in the pulmonary artery and vein. This must equal O2 consumed.
Ficks CO = O2 consumption / ([O2] pulmonary vein [O2] pulmonary artery)
Factors that increase O2 consumption: | afterload, | contractility, | HR, | size of heart (| radius | tension via LaPlaces Law)
Stroke volume The difference b/w end-diastolic volume and end systolic volume; = the volume of blood ejected by the LV during a heartbeat. Varies directly
with contractility and preload; varies indirectly with afterload. Factors affecting SV are below:
Contractility and SV || with: Contractility and SV ++ with:
| Preload and + afterload
Catecholamines (| activity of Ca2+ pump in SR)
| Intracellular Ca2+
+Extracellular Na+
Digitalis (| intracellular Na+ | intracellular Ca2+)
+ Preload and | afterload
|1 blockade
Heart Failure
Acidosis
Hypoxia/Hypercapnia
Ejection
Fraction
Fraction of blood received by the LV (end diastolic volume) that is ejected (SV) and reflects the contractility state of the heart. A larger EF
means more contractility. Normal is 55-80%
EF = SV / LVEDV
and
SV = CO / HR = EDV ESV
Cardiac Cycle
Pressure in
Systole and
Diastole
Diastole: MV opening, LV filling, Pressure |; LA contracts and MV
closes; then LV contracts |LV pressure more AoV opens
Systole: AoV opens, LV ejects blood aorta. The LV
Pressure + and ejection rate slow; AoV closes when LV
Pressure<Ao Pressure. LV: isolvolumetric relaxation; MV
reopens when LVP<LA Pressure.
More
Pressure
Changes
Jugular Venous
Pulses
Provides a complementary pressure tracing to follow mechanical (vs valvular) events of systole and diastole;
consists of a, c, v, waves and y descent. a wave: Atrial contraction; c wave: RV contraction (Tricuspid valve bulges
into RA); v wave: Atrial Filling (|RA pressure b/c filling against closed tricupsid); Y descent: Correspondes to rate
of atrial empyting as TV opens
NB: Y descent slope + in tamponade b/c RA empties slower; | in constrictive pericarditis
LV Pressure In diastole, PLV = PLA until MV closes. During Isovolumetric contraction, PLV rises until > PAo; AoV opens
systole. Then PLV drops as blood leaves; relaxes until it = PLA; then mitral valve opens again
LA Pressure Approximated by the pulmonary capillary wedge pressure (PCWP) measured with a Swan Ganz Catheter.
Aortic Pressure In diastole, PAo > PLV and AoV remains closed. Then PLV > PAo, AoV opens, PAo increases as blood flows into it.
PAo decreases when the ejection rate slows; PLV drops; AoV closes diastole
Normal
Pressure
Right Atrium Right Ventricle Pulmonary Artery Left Atrium Left Ventricle Aorta
<5 mmHg 25/5 mmHg <25/10 mmHg < 12 (about PCWP) 130/10 mmHg 130/90 mmHg
Heart Sounds Sound Significance
S1 MV and tricuspid valve close; MV closes before tricuspid does, so S1 may be split.
S2 AoV and Pulmonary valve close; AoV closes before the pulmonic; inspiration causes || splitting of S2
S3 At end of rapid ventricular filling; normal in children; associated with dilated CHF in adults
S4 Filling of ventricle by atrial systole; not audible in normal adults; suggests high atrial pressure or stiff ventricle.
Heart Sounds
& Inspiration
Inspiration decreases intrathoracic pressure, which increases venous return to the heart and delays pulmonic valve closure (P2 delayed);
blood also wants to stay in the lung due to lower intrathoracic pressure which + venous return tot eh LA and LV, reduces LV filling, and
shortens LV emptying allows the AoV to close early. In paradoxical splitting (as in aortic stenosis) A2 and P2 come closer together during
inspiration.
Arterial
Pressure
Regulation
Systolic Pressure Diastolic Pressure
Highest arterial pressure of the cardiac cycle; measured after he heart
contracts and blood has been ejected into the arterial system; | in older
pts b/c of age related large artery stiffening. | in young pt with | SV.
Decreases (+) with dehydration, |-blockers, diuretics, and blood loss.
Lowest arterial pressure of the cardiac cycle. Corresponds to
time when heart is relaxed and blood is returning to heart via the
venous system. + with aortic stiffening (+ compliance) which
less blood volume in the aorta at the start of diastole.
Pulse Pressure: Systolic Pressure Diastolic Pressure
Difference between systolic and diastolic pressures. Depends mainly on SV. Decreased vessel capacitance due to aging (stiff pipes) |
pulse pressure b/s systolic pressure | while diastolic pressure +

Cardiovascular Physiology
Mean Arterial
Pressure
Defined as Diastolic Pressure + 1/3 * Pulse pressure = DBP + 1/3 * (SBP-DBP) = MAP
Mechanisms to regulate BP: Baroreceptor reflex (short term; in carotid sinus; always active); RAAS (long term); cerebral ischemia
hypercapnia; hypoxia with PO2 < 60 mmHg; Severe volume depletion leading to ADH secretion; atrial stretch mediated by Atrial Natriuretic
Peptide (ANP); and autoregulation.

Changes in MAP are detected either by baroreceptors or the kidney as decreased extracellular circulating volume (ECV). Decreased
baroreceptor firing is centrally processed and relayed to the autonomic nervous system (ANS); and decreased ECV activates the renin-
angiotensin-aldosterone system (RAAS). Baroreceptors are neurally controlled and fast; RAAS is hormonally controlled and slow.
Baroreceptor
Reflex
Stretch receptors in the walls of the carotid sinus and aortic arch respond to MAP and pulse pressure. Carotid sinus baroreceptors are
tonically active: + BP + activity; | BP | Activity. Changes in firing rate transmitted at the carotid sinus (by CN IX) and at the aortic
arch (by CN X) are relayed to the vasomotor system of the brain and elicit ANS response. The sympathetic and parasympathetic nervous
systems affect HR via the SA node, AV node, conduction velocity, and blood vessel tone using action on |1 and muscarinic ACh receptors.
Affected Tissues Sympathetic Parasympathetic
HR, Conduction velocity at AV node, Contractility | via |1 receptor + via mACh receptor (|contractility in atria only)
Vascular Smooth muscle Constriction via o1
Relaxation via |2
N/A
Maneuvers that affect baroreceptor reflex:
|Sympathetic, +Parasympathetic +BP +Baroreceptor to |BP +Sympathetic, |Parasympathetic |BP |Baroreceptor to
|BP
Carotid occlusion, cutting afferents, orthostasis/lying to standing, fluid
loss.
Carotid massage, volume loading, and weightlessness
Renin-
Angiotensin-
Aldosterone
System
Discussed more in renal, BUT: Decreased BP activates the RAAS. Renin is secreted | conversion of angiotensiogen to angiotension I
ACE converts Angiotension I Angiotensin II Adrenals; stimulated synthesis of aldosterone. Aldosterone activates Mineralocorticoid
receptors in the Principal Cells of the Distal Tubule Na+, H2O reabsorption and K+ secretion; also acts on the o-intercalated cells of the
collecting ducts to stimulate H+ secretion to regulate HCO3- levels/acid/base balance. | ECF, |BP
Baroreceptors
& RAAS
Baroreceptor Reflex: Fast RAAS: Slow
Decreased Blood Pressure
Decreased Baroreceptor Firing | Renin angiotensinogen | angiotensin
Brainstem | Aldosterone release
+ Parasympathetic, | Sympathetic outflow to heart + Na+ and + water excretion
|HR, |Contractility, |SV, |Vasoconstriction of arterioles and veins | ECF volume
Increased Blood Pressure
Autoregulation Each organ has a different mechanism to maintain constant blood flow. Except for pulmonary vasculatute, where hypoxiavasoconstriction,
all other organs: hypoxia vasodilation to | delivery of blood and O2. Circulation notes: Liver gets largest share of CO; Kidney gets
highest blood flow per gram of tissue; Heart has largest arteriovenous O2 difference; increased O2 demand is met by | coronary blood flow.
Organ Factors determining Autoregulation %CO
Received
Heart Local metabolites: O2, adenosine, NO; enhanced during mechanical compression in systole 5
Brain Local metabolites: CO2 (pH) 15
Kidneys Myogenic and tubuloglomerular feedback 20
Lungs Hypoxia induced vasoconstriction 100
Skeletal Muscle Local metabolites: lactate, adenosine, K+, His, Bradykinin 20
Skin Sympathetic Stimulation 5
Components
of the
Circulatory
System
Blood Comprises 8% of total body weight. NB: Serum = plasma clotting factors. Blood components:
Blood 55% plasma 91.5% H2O
7% proteins
1.5% salt, lipids, enzymes, vitamins
55% albumin
38% globulins
7% fibrinogen
45%
hematocrit
(formed
elements)
Erythrocytes
Leukocytes
Platelets
PMNs 40-70%
Lymphocytes 20-40%
Monocytes 2-10%
Eosinophils 1-6%
Basophils <1%
Vasculature Composition Pressure Function
Artery Thick walled with elastic tissue, smooth muscle High Deliver oxygenated blood to tissue
Arteriole Smooth muscle with innervation from autonomic
fibers
High Smallest branch of arteries; highest resistance
Capillary Single layer of endothelial cells, thin walled Low Exchange nutrients, H2O, gas w/tissues; | Surface
A
Venule Low Formed from merged capillaries
Vein Thin walled Low The largest vein, the vena cava, returns blood to
heart

Cardiovascular Hemodynamics
Blood Flow
Velocity
Directly proportional to blood flow and inversely proportional to total cross sectional area: higher in aorta, lower in capillaries.
V = Q / A
Where v= velocity, Q=blood flow, A=total cross sectional area
Blood Flow Directly proportional to change in pressure gradient (like Voltage); inversely proportional to blood vessel resistance. Analogous to Ohms law
Q = AP / R
Where Q=blood flow or cardiac output; AP=change in pressure gradient, and R=resistance
Hormonal control: Serotonin arteriolar constriction
Histamine and bradykinin arteriolar dilation, venous constriction: promote flow to site of constriction
Prostaglandins mostly vasodilator Thromboxane A2 vasoconstrictor
Coronary Blood flow: during systole, compress coronary arteries | coronary vascular resistance + coronary blood flow; thus, most
flow happens during diastole
Resistance If Resistance=R, driving pressure=AP, flow=Q, and q=viscosity: then by Poiseuilles law:
R = AP / Q = 8q * Length / (tr
4
)
Viscosity (q) depends on hematocrit, which is increased in polycythemia, hyperproteinemic states (ex: multiple myeloma), hereditary
spherocytosis. Resistance is inversely proportional to the 4
th
power of r; so | r 2x + R by 16.
Resistance in parallel: 1/R = 1/Ra + 1/Rb + 1/Rn (think systemic circulation: everything branching off of the aorta
Resistance in series: R = Rartery +Rcapillaries + Rvein (think, in a single organ)
Capacitance Describes how distensible a blod vessel is; inversely proportional to elastance. Veins are more compliant (less elastic) than arteries, thus
more blood is stored in veins. Aging + compliance.
C = V / P
Where C = capacitance (ml/mmHg); V = Volume; P= pressure
Laminar vs
Turbulent
Laminar flow is in a line; turbulent flow is crazy and causes bruits. Turubulence is increased by + blood viscosity (like anemia) or | blood
velocity (ex: a smaller vessel; increased cardiac output)
Capillary Fluid
Exchange
Fluid mvmt: is a function of osmotic and hydrostatic pressures in the capillary and intersitial space = Starling Forces. Includes:
Pc = Capillary pressure: moves fluid OUT of a capillary Pi = Intersitial pressure: move fluid INTO the CAPILLARY
tc = Plasma colloid osmotic pressure: Moves fluid INTO the capillary tI = Interstitial fluid osmotic pressure: move fluid OUT of
capillaries
Net Filtration Pressure Sum of Starling Forces: Pnet = [(Pc - Pi) (tc - ti)]
Net Fluid Flow Determined by Pnet and Kf (filtration constant/capillary permability): known as the Starling Equation:
Jv = Kf * Pnet = Kf * [(Pc - Pi) (tc - ti)]
A posititve Jv means flow OUT of the capillaries
Lymphatics Almost all lymph of body drains to thoracic duct to venous system; lymph from R upper body right lymph
duct. Lymph has same composition as surrounding interstitial fluid.
Edema Occurs when interstitial fluid volume > lymphatic and filtration capacity. Caused by |Kf, |Pc, or +tc (all |Jv)
Cause Examples
|Pc | venous pressure; standing edema in dependent limbs
+tc + plasma protein b/c: +synthesis (liver disease); +intake (malnutrition); |excretion (nephrotic
syndrome)
|Kf Burn, Inflammation
Types of
Edema
Edema Transudate Exudate
Mechanism |Pc or +tc: fluid from the vessel is either pushed out or
leaves based on pressure differences
More permeable vessels (|Kf): vessel is leakier so both
protein and fluid leave
Composition Protein poor Protein Rich
Electocardiograms
Overview ECGs= recordings of electrical impulses; info about cardiac structure/function. Impulses follow cardiac conduction system:
Electrical impulse at SA node atria AV node slow impulse conduction to allow atrial contraction to finish before ventricular
contraction begins bundle of His right and left bundle branches purkinje fibers which stimulate myocardial cell contraction.
Lead system
and intervals:

Draw lead
position and
ECG
examples!
Twelve leads along set axes: 6 leads on frontal plane: I, II, III, and aVR, aVL, and AVF; and 6 transverse/precordial leads (V1 V6). ECG is
recorded on 1mm graph paper at 25 mm of paper per second. Each small box = 0.04s; each large box = 0.2s.
ECG Defined Normal Range
P wave Atrial depolarization
PR interval Conduction delay through AV node; depends on conduction velocity, HR <200 msec (3-5 box)
QRS complex Ventricular depolarization <120 msec (<3 box)
QT interval Mechanical contraction of the ventricles Corrected <0.45 sec
T wave Ventricular repolarization. T wave inversion = recent MI (atrial repolarization masked by QRS)
ST segment Isoelectric; ventricles are depolarized.
U wave Caused by hypokalemia, bradycardia.
Wolff-
Parkinson-
White
Syndrome
If accessory pathway from the atrium to the ventricle is present, electrical impulses bypass the AV node and ventricles depolarize earlier.
Characteristic delta o wave on ECG just before the QRS; may reentry current supraventricular tachycardia.

Cardiovascular - Arrhythmias
Defined Abnormalities of electrical rhythm that result from abnormal impulse conduction, abnormal impulse formation, or both.
Impulse
Conduction
Problems
May be due to a failure or delay in conduction; often occur in AV node or bundle branches
AV
Block:
degrees
1
st
Conduction bw atria/ventricles delayed due to an abnormal AV node. Prolonged PR interval with a QRS following each P
wave. Due to many causes: vagal stimulation, | blockers, infiltrative or degenerative conditions (amyloidosis, sarcoidosis)
2
nd
Intermittent or cyclical failure of impulse conduction from atria to ventricles. If regular, describe ratio of P:QRS. 2 types:
Type Mobitz Type I Mobitz Type II
Description Intermittent AV conduction failure Sudden, unpredictable AV conduction failure
ECG Finding Progressive PR lengthening until dropped beat
(no QRS after P)
Constant PR intervals before dropped beat
Block site AV node Usu below AV node; assoc w/bundle branch block
Complications Usu asymptomatic; rarely progress to 3
rd
d block Often progresses to 3
rd
d block; may need
prophylactiv pacing
3
rd
Complete block: failure of any impulses to be conducted from atria to ventricles. Atria and ventricles beat independently of
each other (AV dissociation); both P and QRS present, but no relationship b/w them. Atrial rate> ventricular rate. Needs
pacemaker.
Bundle
Branch
Block
Failure of impulse conduction through one of the bundles affected ventricle depolarizes more slowly. Ex: In LBBB, the RV
depolarizes before the LV.
Impulse
Formation
Problems
Due to ectopic impulse originating from outside the SA node; depolarizes heart ectopic beat. May come from latent pacemaker cells (in
AV or His-Purkinje; escape beats); from the atria (supraventricular arrhythmia); or from the ventricles (ventricular arrhythmia).
Escape Beats &
Rhythms
Nodal/Junctional
Escapre Beats
Originate from AV nodal area His purkinje system to ventricles normal QRS. Can be seen in
complete 3
rd
d AV block. Typical rate: 45-60/min
Ventricular
Escape Beats
Originate from ectopic ventricular focus, like purkinje fibers. Abnormal QRS. Can be seen in
complete 3
rd
d AV block. Typical rate: 35-40/min
Supraventricular
Arrhythmias

(from atria or AV
node; normal
QRS)
Paroxysmal
Supraventricular
Tachycardia
Regular, rapid (150-250/min) arrhythmia that originates in atria or AV node; often due to reentrant
pathway in the AV node.
Atrial flutter Regular, rapid (250-350/min) arrhythmia from the atria. ECG: rapid succession of identical atrial
depolarization waves = sawtooth appearance. Caused by re-entry over a large fixed circuit; not all
impulses are transmitted to ventricles b/c of AV node refractory period: 2:1 or 4:1 conduction
Atrial fibrillation Irregularly irregular, rapid (350-600/min) impulses from multiple atrial foci that depolarize atria.
Chaotic and erratic baseline with no discrete P waves and irregularly spaced QRS. Associated
with R or L atrial enlargement. Ineffective atrial contraction + CO
Ventricular
Arrhythmias
(abnormal QRS
complexes; from
ventricles)
Premature
Ventricular
Contraction
Ectopic ventricular pacemaker produces an ectopic beat before the next sinus beat occurs. Abnormal
QRS (slow impulse conduction through ventricular myocardium)
Ventricular
Tachycardia
Ectopic impulses from ventricles regular, rapid rate (100-250/min). Usu caused by a re-entry
mechanism. Can deteriorate to ventricular fibrillation. Torsade de pointes is a form of VT in which QRS
amplitude and axis change cyclically. Occurs in pts with prolonged QT interval (congenital defects are
due to defect in sodium or potassium channels; present with sensorineural deafness; includes Jewell and
Lange-Nielsen syndrome)
Ventricular
fibrillation
Rapid, irregular ventricular depolarization due to impulses from multiple ectopic ventricular foci.
Completely erratic rhythm; no identifiable waves. Fatal without immediate defibrillation.