3.

9
Cardio Perpheral circ (blood flow) & Cardiac mm (elec activity and mm
dynamics)

Peripheral Circulation
2 pumps and 2 circuits

Blood flows from HIGH pressure to LOW pressure - allows blood to flow from aorta
back to R. atrium.

Ex. In R ventricle failure, there is a build up of blood, backing up into R. atrium,
therefore the pressure increases from 0. And then Net system will get decreases,
causing edema since blood cant reach back up to heart due to a decrease in the
pressure.




3.10
In which part of sys circuit would u expect greatest systemic drop? In Arterioles!!
Apprx 40 mL

Which part has greatest cross sectional area? CAPILLARIES. Smallest cross
sectional? Aorta

Highest velocity? Aorta . Smallest radius, GREATER Velocity. ONE AORTA, manyyy
capillaries added together. Lowest velocity is in cap. for exchange to happen!!

Largest blood vol is in sys veins. 2
nd
largest in pul sys.




3.11
Hemodynamics

Flow Q= P1-P1 / R

R = Viscosity x Length / radius^4

Q = delta P x r^4 / V x L

Magic number for flow 16 times increase !!! When the heart is occluded by 50% !
2x2x2x2

Most imp factor that affects flow is resistance

Types of Flow:
Laminar of Turbulent Flow
Laminar flow is in layers! Layer with HIGHEST velocity is in the center of the tube

Turbulent Flow non-layered flow. Creates murmurs aka turbulance. MORE
resistance against flow!

Reynolds number = diameter x velocity x density / viscosity of blood
>2000 = turbulent flow
<2000 = laminar flow

Resistance 2 types
Series and Parallel

In series, flow goes from one to another. R1 R2 R3.
Flow is DEPENDENT, equal at all points

Series Flow is dependant
If flow is decreased in one part, it will decrease in ALL, since they are in
series. Clinical decrease flow in one part of pt, all parts connected in series
will also decrease in flow.

Parallel flow is independent. Total resistance is calculated in reciprol 1/RT =
1/R1 + 1/R2 + ** the more resistance u ADD, the LESS total resistance u get
ADD TO GET LESS!
SUBTRACT to get MORE!




4.1
Kidney donor:
Organs are all parallel

If R = dec, then Total R= Inc,
Then, Q = Dec, Cardiac Output = Dec

Chart on 13 min !!!!!!!!! REDO!!!!!

2 organs connected in parallel

Greatest to least resistance (lowest to highest flow): coronary, cerebral, renal,
pulmonary

4.2
Laplace relationship: tension in a vessel is proportional to pressure x radius
Aorta greatest radius and LARGEST wall tension. With aneurysm, incr radius.

Compliance = change in vol / change in pressure
Compliance is inverse to elasticity and recoil
MORE elasticity, LESS compliance .

Arteries have MORE mm, then veins. N more mm = more elasticity (less compliance)


4.3
Sys veins 20x more compliant than arteries. Veins also store 70% of blood because
of higher compliance.

Constricting the veins = decrease radius, and increase venous return.



4.4
Characteristics of Sys Arteries
Systolic contraction and pushing blood into aorta
Dyastolic relaxed state during diastole
Pulse Pressure = Sys Dia = 40

Mean arterial pressure = S+D / 2


Factors affecting sys pressure -> MAP = CO x total peripheral resistance ***

( CO = HR x Stroke Vol. ) -> dep on SYS activity & TPR represents dia

To increase TPR, decrease radius, drug that constricts

Pulse pressure = S-D
To incr PP, either increase S, or decrease D. Increase S by incr CO ( Incr. HR)
To dec. D = decr TPR, incr radius

**** Low compliance = Inc S, dec D


4.5
Factors Affecting Dia pressure
To decrease.
1) a dec in TPR
2) a dec in HR, if CO is reduced
3) a dec in stroke vol.
4) dec in vessel compliance

Factors Affecting Pulse Pressure
-inc = sys inc and dia decr


Factors Affecting Mean Pressure
**Mean Press = diastole +1/3 pulse pressure**

M art.P = CO x TRP !!!!

P.P increases as we go distally (HAND), Compliance increases as we go centrally
(HEART)
Compliance inverse to PP

Hemorrhage losing blood vol.
During exercise, dec TPR, Increase CO, therefore MAP remains normal, but if
someone has a problem in their arterial resistance, for example, arthersclorisis, then
their arteries will be still and they will have a problem decreasing TPR, therefore
will get a HIGH MAP.


4.6 Effect of Gravity

Arteries always have more pressure than veins. Highest absolute pressure will be
found in the lowest artery listed

Orthostatic hypotension when blood pressure decreases because a person goes
from supine to upright position


4.7 Effects of Intrapleural pressure on pulmonary blood flow and volume

during inspiration, blood pressure falls. Pressure is inverse to Volume.
Inspiration pressure more negative
Expiration more positive (increases). Venous return and output of R ventricle are
decreased.



4.8
diffusion formula

factors that affect change from a capillary. When substances LEAVE = filtration (+).
ENTER cap = reabsorption (-)

Exchange hydrostatic (p) due to presence of water, a pushing force.
Oncodic (pi) due to proteins, a pulling force

***
Inside cap Pc (+) Outside cap Pif (-)
c (-) if (+) Increase filration? + !


ADD n Subtract to get EXCHANGE!!



4.9
Ascitis in pt liver is fucked, so protein inside cap is decreased, therefore
reabsorption of water is decreased!

Nephrotic syndrome pt would have protein urea. Pt cannot reabsorp, leading to
edema due to a DECREASE of oncotic pressure in capillary

Pt with 3
rd
deg burn in 25% of body. Burn ALLLL the way down to dermis, leading to
breakage to capillary beds leading to LOSS of proteins =Increasing oncotic pressure,
pulling fluids AWAY from capillary. Must give heavy fluid to increase colodial
pressure in capillaries.

Ch summary.



4.10 Measurement of CO
For vessel use poselles
For flow thru an organ Ficks formula Flow=Uptake / A - V ********



4.11 Regulation of blood flow

Intrinsic regulation (autoregulation blank cheque to pay theirselves)
- brain, heart, exercising mm (myogenic stretch receptors and metabolic
vasodilatory metabolites). The favoured is metabolic**
- In brain, PaCo2 ..
-In heart, adenosine
-In exercise mm, lactic acid !!

DINOSAUR STORY brain, heart, exercise mm control their own blood flow



Extrinsic
Brain = ANS skin and resting mm

Alpha 1 receptors when stimulated they will constrict of blood vessels. When u
inhibit them, dilation will take place

Beta 2 receptors stimulate= cause dilation, when inhibit cause constriction.

In RESTING mm to constrict: (+) a1, (-) b2
To dilate: (-)a1, (+)b2
NO effects of parasymp of blood flow n resting mm .

Skin and resting mm, ANGIOTENSIN II (+) = constriction

Factors affecting TPR = radius > sym a1 and b2 and angiotensin

During exercise, blood flow in BRAIN remains SAME!!! Also, blood pressure in lung
will remain SAME in normal person.



5.1
when exercising, Adenosine is produced where the heart works.
Adenosine increases flow to heart and coronary flow increases. Heart receives 5-
10% CO, whereas kidney 20%

During systole, the LEFT side of the heart received MINIMAL flow, but right side
(weaker pump). But during diastole, no compression, MAX flow. Heart FEEDS itself
during diastole. Any disease affecting diastole, affects a lot.

Hypertension a few years without treatment will lead to death.


5.2
Flow is proportional to arterial PCO2. Normal person, increase in oxygen, no change,
decrease in oxygen there will be an increase in cerebral blood flow.

Temperature regulation
Alpha 1 is dominant in controlling flow to skin

To increase heat in our body = decr flow to skin = constricting vessels a1(+)

Pt w/ heat exhaustion or fever.. u want to increase flow to skin, therefore must
dilate so (+) b2 and (-)a1

Pt with hypothermia, u want to decrease flow to skin, therefore constrict vessels,
(+)a1, and (-)b2 = shivering

Lung is a low pressure circuit, because it is very compliant.

Pulmonary response to hemorrhage = a large decrease in cardiac output means decr
volume pumped into circuit = decr in pulm pressures


5.3 Fetal Circulation
PDA, what would happen to oxygen content? increases
Which part of fetal circulation would you expect to have highest O2 content?

Umbilical vessels -> R.A -> RV (Major Pump 25 mmHg) ->Pul A ductus arteriosis
AORTA sys circulation

In adults, from Pul A LUNGS ->LALV (100 mmHg) THEN aorta (this is
surpassed because lungs are collapsed in fetus.

When born, ductus arteriosis closes, and the LV starts working as pump. If duct does
not close, Patent D.A., will cause back flow of blood BACK to PA

4 Congenital conditions that cause CYNOSIS all begin with T !!!
1. Tetrology of Fallot
2. Truncus Arteriosis
3. Transposition of great vessels
4. Tricuspid atresia

RECAP



5.4 Cardiac mm
peripheral circulation and cardiac mm.

Cardiac mm
- 1) electrical activity action potentials. 2 kinds: 1) ventricle mm 2) SA node
o Ventricle AP:
Ions Na (low perm.), K(high) , Ca (low)(similar to skeletal, both
have Na and K)
Channels
Voltage fast (Na) and slow (K) channels
Un-Gated (K) always open
- 2) mechanic






5.5 Membrane Channels
1. Ungated K channels ALWAYS open
2. Voltage gated (dep) Na channels are CLOSED under resting conditions. They
open during membrane depolarization.
3. Voltage-gated K channels Closed under resting conditions.
Inward rectifying, iK1 = open when resting

Delayed rect., iK-, open with depolarization and closes when cell is
repolarized.


5.6
phase 0 = caused by NET influx of Na+, depolarizing cell means MORE positive!!
Phase 1 = slight REpolarization, slightly more negative. Net EFLUX of K
Phase 2 = prolonged.. plateu phase. CONSTANT. Influx of Ca ions, balanced of efflux
of K ions creating almost eqm. APD = absolute refractory period is wide, if
stimulus is given, NO other AP can occur
Phase 3= rapid repolarization, net efflux of K ions, losing positive, becoming neg
Phase 4 = back at resting, slowww efflux of K. both K channels are open


Channels available:
Phase 0: Na channels open quick then close quickly (fast channels). K-gated are
CLOSINGGG not completely closed!!!!
Phase 1: ungated K channels. Gated K are closedd
Phase 2: K channels closed. But K leaving thru ungated channels.



5.7 Elect vs. Mech events

SM VM
1. Na closed @rest 1. same
2. K ungated always open 2.same

3. no Ca channels 3.Ca !!
4. K volt closed @rest 4. open @rest .. increases ARP and
APD, therefore cant tetanize heart
mm.

Can only generate another AP during relative refractory period


5.8
Heart SA node action potential
SA node pace maker of heart, has automaticity, generates its own beat from brain
via ANS. Brain tells the heart to beat

3 phases
phase 0 : Ca !!!!!! special depolarization ***
phase 3: efflux of K (similar to VM)
phase 4: slowww depolatization, cells are slowlyyy going more positive. Hypothesis:
due to a slow influx of Na OR due to a slow influx of Ca OR due to an increasing
conductance (decrease efflux) of K.

Effect of Sympathetics on SA node affects at phase 4!! By increasing influx of Na or
Ca or decr efflux of K. Increases the slope of depolarization = increase HR

SYMP INCREASE HEARTRATE**** -- since it affects phase 4!!

Parasymp affects at phase #!! Increases conductance of K, leading to
hyperpolarization. NET: decrease HR!!


SA node atrial mm AV node (delay) purkinje fibers Ventr mm

Fastest conducting fiber: purkinje SLOWEST vel = AV node

Automaticity
SA node: Highest intrinsic rate
AV:2
nd
highest
Purkinje: Slowest intrinsic rate


5.9 EKG
comprises of PQRS complex

P wave atrial Depolarization. SA node sends
QRS vent depolarization
T vent repolarization

Which phase in the vent action potential best represents QRS in EKG? Phase 0
represents T wave in EKG? Phase 3


5.10
QRS duration shud b less than 0.12 sec
QT indicates vent refractoriness 0.35-0.44
Hypercalcemia = shortened QT
HYPOcalcemia = prolonged QT
Digitalis =shortened QT


Estimation of Heart Rate
1. Interval Method:
2. beats per min. 3 beats in 3 seconds. So 3/60=20 x4 = 80 beats per min




5.11 Heart Block

First degree heart block slowed conduction thru the AV node. PR interval
increased (measure of conduction thru AV node Norm )


Second Degree block side of highway some not all are pulled over.
A missing QRS


Third Degree heart block no impulses are conducted from atria to ventricles. Heart
beat will become Asynchronous a loss of pattern

Atrial Flutter
saw tooth repeated p waves

Atrial Fibrillation
No dicernable p wave. QRS irregularly spaced

Ventricular Fibrillation
No identifiable QRS rhythm.


Einthovens Triangle ****** REMEMBER
Normal axis of heart -30 and +110
Left Axis deviation -30 to -90
- Can be caused by left vent hypertrophy, conduction def of left vent, acute MI on R
side tends to shift axis to left
Right Axis deviation +110 to +180

Evolution of an Infarct ********??????



6.1
Heart Mechanics

Performance of the heart depends on Pre-Load and Contractility
- Preload is when mm is being stretched
o During DIASTOLE
o To decrease preload: give diuretic or ACE inhibitors
o To increase end diastolic vol: give Albumin based fluid
- Contractility any change in performance at the same preload
o When there is an increase in performance but no increase in preload
o To measure contractility
Ejection Fraction = EDV ESV / EDV = SV / EDV
EF in normal heart is 2/3 !!
dp/dt changes =invasive
digoxin increases contractility = interfere w/ membrane
transport, and also relaxes faster


6.2 Indices of Contractility

Increase contr = decrease systolic interval , increase HR = dec diastolic interval

Systolic interval decreased: contractility effect
Diastolic interval decreased: heart rate effect

6.3
CARDIAC FXN CURVES ** ???


6.4
Vascular CURVE



6.5
Factors that affect contractility AFTERLOAD (after contraction. Force that mm
must generate to eject blood into aorta

Hypertension: increased afterload .. curve moves to LEFT, heart has to compensate
Hypotension: decreased afterload

End diasolic vol vol of blood in vent at end of diastole
End sys ..:vol of blood in vent at end of sysyole
Stroke vol: vol of blood ejected by venticle per beat
SV = EDV ESV
Residual vol: vol of blood in ven after MAX contraction

****EDV proportional to preload
***ESV is INVERSE to contractility (increase 1, other decreases)


Control of Heart Rate and Blood Pressure
- blood pressure dep on 2
o hormones Aldosterone, ADH, Atrial Neuritic Peptide
o ANS
Symp (more dom. role) Increases HR. Affects phase 4!!! ***
Affects blood vessels in skin, mm by alpha1 and B2
o Cause an increase in TPR
Parasymp Decreases HR Affects SA node at phase 3 !!

MAP = CO x TPR ****



6.6
blood pressure 9, 10 CNs
afferent fibers take problem from carotid sinus and aortic arch to MEDULLA.. If
firing rate of afferent fibers are overfiring then it means increase in blood pressure.
Brain finds solution.

Medulla 4 min chart Symp vs Parasym
- major hormone players: rennin and angiotensin 2 (increase aldosterone)

Solution
Carotid Massage!! - fooling body as if blood increase.

And when getting up too fast from supine, sympathetics are delayed so u feel dizzy

Weightlessness: astornauts blood is immedietly shunted over, cause increase in
circulating vol. = inc venus return = increase in BP.!!! Brain helps?
- up para, down symp..


6.7 Cardiac Cycle

Graph axis . TOP = pressure, mL, BOTTOM = time

EKG at bottom P wave = atrial dep.

QRS closure of MITRAL VALVE !!!! ends diastole and begins sys.

Fists Pwave top fist close, QRS bottom first close

Lub sys, closure of mitral, dub dist, close of aortic valve

***Murmurs could be sys: due to abstruction of Aortic Stenosis, mitral
insufficientcy
- dias: aortic insufficientcy, mitral stenosis
Suspect??? Get ventricle pressure tracing (has a graph)



6.8
-

- pressure
o vent (>120 Norm**), if increases more=
aortic valve path
Press gradient between the peak vent pre and aortic pre =
obst=Aortic Stenosis
No pressure gradient = regurg = A.I.
o atrial (>15 Norm***).. if increases more =
mitral valve path
If UP in diastole = obst = MS
If UP in systole = regur =MI
o In graph: first D then S

7.1
Venous pressure tracing


A wave =contraction of R. A
C wave = bulging of tricuspid, near beginning of vent contraction
V wave = R. atrial filling
Y descent =rapid fall of atrial pressure when tricuspid opens

Volumes
NORM: EDV = 125, ESV =50, SV = 75, EF= 125/75=0.60

Changes in preload, will not primarily change ejection fraction, but contractility
does!!!

Pressure volume loop
Most o2 is being utilized during isovol contraction!!
Most work is done? When there is movement !!!

Pause: -15:56